Wave Life Sciences Corporate Presentation May 3, 2023 Exhibit 99.2

Forward-looking statements This document contains forward-looking statements. All statements other than statements of historical facts contained in this document, including statements regarding possible or assumed future results of operations, preclinical and clinical studies, business strategies, research and development plans, collaborations and partnerships, regulatory activities and timing thereof, competitive position, potential growth opportunities, use of proceeds and the effects of competition are forward-looking statements. These statements involve known and unknown risks, uncertainties and other important factors that may cause the actual results, performance or achievements of Wave Life Sciences Ltd. (the “Company”) to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements. In some cases, you can identify forward-looking statements by terms such as “may,” “will,” “should,” “expect,” “plan,” “aim,” “anticipate,” “could,” “intend,” “target,” “project,” “contemplate,” “believe,” “estimate,” “predict,” “potential” or “continue” or the negative of these terms or other similar expressions. The forward-looking statements in this presentation are only predictions. The Company has based these forward-looking statements largely on its current expectations and projections about future events and financial trends that it believes may affect the Company’s business, financial condition and results of operations. These forward-looking statements speak only as of the date of this presentation and are subject to a number of risks, uncertainties and assumptions, including those listed under Risk Factors in the Company’s Form 10-K and other filings with the SEC, some of which cannot be predicted or quantified and some of which are beyond the Company’s control. The events and circumstances reflected in the Company’s forward-looking statements may not be achieved or occur, and actual results could differ materially from those projected in the forward-looking statements. Moreover, the Company operates in a dynamic industry and economy. New risk factors and uncertainties may emerge from time to time, and it is not possible for management to predict all risk factors and uncertainties that the Company may face. Except as required by applicable law, the Company does not plan to publicly update or revise any forward-looking statements contained herein, whether as a result of any new information, future events, changed circumstances or otherwise.

Emerging leader in RNA medicines Multi-modal drug discovery and development platform to address new areas of disease biology RNA editing, splicing and silencing Differentiated, clinical-stage RNA medicines pipeline with first-in-class RNA editing programs Strategic collaborations to expand and advance pipeline (GSK and Takeda) Multiple pipeline and platform catalysts expected in 2023 and beyond Well-capitalized with expected cash runway into 2025 GMP manufacturing Strong and broad IP position1 Wave Life Sciences is an RNA medicines company committed to delivering life-changing treatments for people battling devastating diseases 1stereopure oligonucleotides and novel backbone chemistry modifications 3

RNA medicines allow matching disease target to therapeutic modality Silencing Splicing RNA Base Editing Degradation of RNA transcripts to turn off protein production Restore RNA transcripts and turn on protein production Efficient editing of RNA bases to restore or modulate protein production Endogenous ADAR enzyme Restored Reading Frame Endogenous RNase H Endogenous AGO2 RISC Functional Protein Skip

Program Discovery Preclinical Clinical Rights Patient population (US & Europe) RNA EDITING WVE-006 SERPINA1 (AATD) GSK exclusive global license 200K Multiple undisclosed 100% global - SPLICING WVE-N531 Exon 53 (DMD) 100% global 2.3K Other exons (DMD) 100% global Up to 18K SILENCING: ANTISENSE WVE-003 mHTT (HD) Takeda 50:50 Option 25K Manifest (SNP3) 60K Pre-Manifest (SNP3) WVE-004 C9orf72 (ALS and FTD) Takeda 50:50 Option 4K (C9-ALS) 26K (C9-FTD) SCA3 (ATXN3) Takeda 50:50 Option 8K SILENCING: RNAi Undisclosed 100% global - Robust RNA medicines pipeline with first-in-class RNA editing programs Through GSK collaboration, Wave can advance up to three collaboration programs and GSK can advance up to eight collaboration programs Phase 1/2 Phase 1/2 Phase 1/2 AATD: Alpha-1 antitrypsin deficiency; DMD: Duchenne muscular dystrophy; HD: Huntington’s disease; ALS: Amyotrophic lateral sclerosis; FTD: Frontotemporal dementia; SCA3: Spinocerebellar ataxia 3

WVE-N531 Duchenne muscular dystrophy

Duchenne muscular dystrophy Genetic mutation in dystrophin gene prevents the production of dystrophin protein, a critical component of healthy muscle function Impacts approx. 1 in every 5,000 newborn boys each year; approx. 20,000 new cases annually worldwide  Approx. 8-10% are amenable to exon 53 skipping Dystrophin protein established by FDA as surrogate endpoint reasonably likely to predict benefit in boys1 for accelerated approval in DMD Increasing amount of functional dystrophin expression over minimal amount shown with approved therapies is expected to result in greater benefit for boys with DMD 1Vyondys: www.fda.gov; viltepso; www.fda.gov; Exondys; www.fda.gov; Amondys: www.fda.gov Dysfunctional Splicing Exon Skipping No dystrophin protein produced Functional dystrophin produced Translation halted Translation continues Mutant pre-mRNA Disease State Restored State mRNA with disrupted reading frame Restored mRNA Mutant pre-mRNA Skip Oligo 53 53 50 51 54 55 50 51 54 55 53 50 51 54 55 50 51 54 55

Preclinical data supported advancing WVE-N531 to clinical development Kandasamy et al., 2022; doi: 10.1093/nar/gkac018 PN chemistry improved function and survival in dKO mice WVE-N531: Dystrophin restoration of up to 71% in vitro Western Blot normalized to primary healthy human myoblast lysate Conc (uM) % Dystrophin Dystrophin Vinculin 100% survival at time of study termination Restored muscle and respiratory function to wild-type levels Note: Untreated, age-matched mdx mice had 100% survival at study termination [not shown] Time (weeks) PS/PO/PN 150 mg/kg weekly PS/PO/PN 75 mg/kg bi-weekly PS/PO 150 mg/kg weekly PBS Survival probability (%) Tidal volume Age (days) TVb (ml) Wild-type dKO: PBS dKO: PS/PO/PN Wild-type dKO: PBS dKO (PS/PO/PN oligonucleotide)

In multidose portion of study, patients received three biweekly 10 mg/kg doses Initial cohort Boys with DMD amenable to exon 53 skipping 1 mg/kg 3 mg/kg 6 mg/kg 10 mg/kg Single ascending intra-patient doses Multidosing at 10 mg/kg every other week Weeks Dose WVE-N531 Period before initiating multidosing (~1 – 2 months) 10 mg/kg 10 mg/kg 10 mg/kg 0 2 4 6 Muscle Biopsy Data include: WVE-N531 muscle concentrations WVE-N531 localization Exon skipping Dystrophin protein

WVE-N531 in DMD: Delivered positive proof-of-concept data in 4Q 2022 Patient Tissue Source Tissue concentration (µg/g) % Exon skipping by RT-PCR Dystrophin by Western blot (% of normal) 1 Deltoid 85.5 61.5 0.24 2 Deltoid 33.5 49.8 0.23 3 Bicep 8.3 47.9 0.34 Mean exon skipping: 53% Mean muscle concentration: 42 µg/g Mean dystrophin: 0.27% of normal (BLQ) High exon skipping and muscle concentrations after three biweekly 10 mg/kg doses Similar exon skipping regardless of mutation Patient 1: del48-52 Patient 2: del45-52 Patient 3: del51-52 PK analysis indicated 25-day half-life in plasma WVE-N531 appeared safe and well-tolerated Data presented March 22, 2023 at Muscular Dystrophy Association Clinical and Scientific Conference Biopsies collected ~2 weeks post-last dose (3 biweekly doses of 10 mg/kg) 42 µg/g = 6.1 µM BLQ: Below level of quantification (1%) Data cut-off: December 6, 2022

Initiating Part B, a potentially registrational Phase 2 clinical trial of WVE-N531 Design: Phase 2, open-label, 10 mg/kg every other week, up to 10 patients  Endpoints: Dystrophin (powered for >5% of normal), safety/tolerability, pharmacokinetics, functional assessments (incl. NSAA and others) Biopsies:  After 24 weeks of treatment After 48 weeks of treatment Data from Part B expected in 2024 Screening Safety Follow-up Biweekly Dosing (10 mg/kg IV) Functional assessment Biopsy after 24 weeks of treatment Functional assessment Biopsy after 48 weeks of treatment Functional assessment IV: intravenous; NSAA: North star ambulatory assessment

GSK Collaboration and WVE-006 for Alpha-1 antitrypsin deficiency (AATD)

Collaboration leverages Wave’s unique stereopure, PN-chemistry containing PRISMTM platform, including editing, splicing, silencing (RNAi and antisense) Strategic collaboration with GSK to develop transformative RNA medicines for genetically defined diseases 1$120 million in cash and $50 million equity investment received in January 2023, 2Initiation, development, launch, and commercialization milestones for WVE-006 and programs progressed during initial 4-year research term (8 GSK collaboration programs) 3GSK eligible to receive tiered royalty payments and commercial milestones from Wave First-in-class RNA editing program GSK granted exclusive global license to WVE-006 for AATD  GSK to advance up to eight collaboration programs Up to $225 million in development and launch milestones Up to $1.2 billion in aggregate in initiation, development and launch milestones Up to $300 million in sales-related milestones Up to $1.6 billion in aggregate in sales-related milestones Double-digit tiered royalties as a percentage of net sales up to high-teens Tiered royalties as a percentage of net sales up to low-teens Development and commercialization responsibilities transfer to GSK after completion of first-in-patient study Development and commercialization responsibilities transfer to GSK at development candidate Wave to advance up to three wholly owned collaboration programs (or more pending agreement with GSK) 3 Wave to leverage GSK’s genetic insights Multiple value drivers to Wave Milestone / royalties Genetic targets Milestone / royalties $170 million upfront to Wave (cash and equity1) Additional research support funding Potential for up to $3.3 billion in milestones2 Expands Wave’s pipeline Extends cash runway into 2025

3) Retain M-AAT physiological regulation 2) Reduce Z-AAT protein aggregation in liver WVE-006: Designed to correct mutant SERPINA1 transcript to address both liver and lung manifestations of AATD M-AAT reaches lungs to protect from proteases M-AAT secretion into bloodstream AAT: Alpha-1 antitrypsin Strnad et al., 2020 N Engl J Med 382:1443-55; Blanco et al., 2017 Int J Chron Obstruct Pulmon Dis 12:561-69; Remih et al., 2021 Curr Opin Pharmacol 59:149-56. WVE-006 ADAR editing approach to address key goals of AATD treatment: RNA correction replaces mutant Z-AAT protein with wild-type M-AAT protein Z-AAT 1) Restore circulating, functional wild-type M-AAT I(G) A SERPINA1 Z allele mRNA encodes Z-AAT protein with E342K mutation Edited SERPINA1 mRNA enables wild-type M-AAT protein production WVE-006 (GalNAc-conjugated AIMer) WVE-006 designed to correct Z allele mRNA to enable M-AAT protein to be produced

WVE-006 in AATD: First-in-class RNA editing candidate approaching the clinic Potentially comprehensive approach to address both lung and liver manifestations of AATD Increased AAT protein in NSG-PiZ mice Demonstrated functionality of M-AAT protein Confirmed restored wild-type M-AAT protein WVE-006 treatment results in serum AAT protein levels >11 uM in NSG-PiZ mice Overall percentages of serum AAT protein isoforms in NSG-PiZ mice (Week 13) Serum neutrophil elastase inhibition activity in NSG-PiZ mice AATD: Alpha-1 antitrypsin deficiency; M-AAT protein: wild-type AAT protein; WVE-006 administered subcutaneously (10 mg/kg bi-weekly) in 7-week old NSG-PiZ mice (n=5 per group); Loading dose: 3 x 10 mg/kg at Day 0. Left: Liver biopsies collected at wk 13 (1 wk after last dose) and SERPINA1 editing quantified by Sanger sequencing; Right: Total serum AAT protein quantified by ELISA; Stats: Two-Way ANOVA with adjustment for multiple comparisons (Tukey) CTA submissions for first-in-human study expected in 2H 2023

Early lead pre-optimization AATD AIMer (SA1-5) administered in huADAR/SERPINA1 mice (8–10 wKs old); lower left: 20x liver images PAS-D stained, 19 weeks; Quantification of PAS-D positive staining, Stats 2-way ANOVA; Right: Quantification lobular inflammation grade (Grade based on # of inflammatory foci in lobules: Grade 0: 0; G1 1-5; G2 6-10; G3 11-15; G4 ≥16) and mean globular diameter (40 largest globules/ animal) with HALO. Stats Wilcox rank-sum tests Early lead (pre-optimization) AATD AIMer reduces aggregation of Z-AAT and inflammation in mouse liver Lobular inflammation (19 weeks) * p=0.03 Inflammation grade PBS AIMer p<0.01 Mean diameter (mm) PBS AIMer **** p<0.0001 Weeks following first dose ** %PAS-D positive area (mean±sem) PBS Early lead AATD AIMer

RNA editing only detected at PiZ mutation site in SERPINA1 transcript (mouse liver) RNA editing across transcriptome (mouse liver) AIMer-directed editing is highly specific in mice SERPINA1 (PiZ mutation site) % Editing Dose 3x10 mg/kg (days 0, 2, 4) SC with AATD AIMer (SA1 – 4). Liver biopsies day 7. RNA-seq to quantify on-target SERPINA1 editing, to quantify off-target editing reads mapped to entire mouse genome; plotted circles represent sites with LOD>3 (N=4), SERPINA1 edit site is indicated No bystander editing observed on SERPINA1 transcript Coverage Coverage Editing site (PiZ mutation) PBS AATD AIMer C 0% T 100% C 48.2% T 51.8%

WVE-004 Amyotrophic Lateral Sclerosis (ALS) Frontotemporal Dementia (FTD)

C9orf72 repeat expansions: One of the most common genetic causes of ALS and FTD Typically 100’s-1000’s of GGGGCC repeats Amyotrophic Lateral Sclerosis (ALS) Frontotemporal Dementia (FTD) Hexanucleotide (G4C2)- repeat expansions in C9orf72 gene are common autosomal dominate cause for ALS and FTD Different manifestations across a clinical spectrum Fatal neurodegenerative disease  Progressive degeneration of motor neurons in brain and spinal cord C9-specific ALS: ~2,000 patients in US Progressive neuronal degeneration in frontal / temporal cortices Personality and behavioral changes, gradual impairment of language skills C9-specific FTD: ~10,000 patients in US Including patients with C9-associated ALS, FTD or both Sources: Balendra et al, EMBO Mol Med, 2017; Brown et al, NEJM, 2017, DeJesus-Hernandez et al, Neuron, 2011. Renton et al, Neuron, 2011. Zhu et al, Nature Neuroscience, May 2020, Stevens et al, Neurology 1998

Target engagement in patients supported advancing FOCUS-C9 clinical study WVE-004 in C9-ALS/FTD: Successful translation of preclinical data to clinic PK/PD modeling using preclinical in vivo models predicted pharmacodynamically active starting dose Additional single- and multi-dose biomarker and safety clinical data expected in 1H 2023 from following cohorts: 20 mg single dose 30 mg single dose 60 mg single dose 10 mg monthly dosing 10 mg quarterly dosing PK: pharmacokinetic PD: pharmacodynamic; Right: Mixed model for repeated measures used to estimate geometric mean ratio to baseline via least squares mean and to calculate p-values. P-values represented by asterisks are for within-dose group geometric mean ratios. *p≤0.05, **p≤0.01, ***p≤0.001. Poly(GP) assay: Wilson et al., 2022 J Neurol Neurosurg Psychiatry doi:10.1136/jnnp-2021-328710. Data cut-off: March 24, 2022

WVE-003 Huntington’s Disease

Healthy individual Huntington’s disease mHTT toxic effects lead to neurodegeneration; loss of wtHTT functions may also contribute to HD Stresses wtHTT Stresses wtHTT mHTT + ~50% decrease in wtHTT Healthy CNS function Synaptic dysfunction | Cell death | Neurodegeneration Loss of wtHTT functions Huntington’s disease (HD) Wild-type HTT (wtHTT) is critical for normal neuronal function Expanded CAG triplet repeat in HTT gene results in production of mutant huntingtin protein (mHTT) HD is a monogenic autosomal dominant genetic disease; fully penetrant and affects entire brain Fatal disease characterized by cognitive decline, psychiatric illness, and chorea 30,000 people with HD in the US and more than 200,000 at risk of developing HD

WVE-003: First-in-class allele-selective candidate for HD mHTT protein levels Placebo WVE-003 (30 and 60 mg pooled*) wtHTT protein levels Reductions in mean CSF mHTT and preservation of wtHTT observed in pooled analysis of single dose cohorts in SELECT-HD clinical study Single dose of WVE-003 Single dose of WVE-003 mHTT protein reductions observed in single dose cohorts (Sep. 2022) wtHTT protein levels appear consistent with allele-selectivity Generally safe and well-tolerated Additional single-dose and multi-dose biomarker and safety clinical data expected in 2H 2023 Reduction in mHTT protein: 22% from baseline 35% vs. placebo mHTT: mutant huntingtin protein; wtHTT: wild-type huntingtin protein *Pooled considering no apparent dose response between 2 cohorts; Data cut-off: August 29, 2022

AIMers RNA base editing capability

Proof-of-concept preclinical RNA editing data published in Nature Biotechnology (March 2022) Monian et al., 2022 published online Mar 7, 2022; doi: 10.1038.s41587-022-01225-1 SAR structure-activity relationship Specificity in vitro & in vivo (NHPs) In vitro-in vivo translation (NHPs) GalNAc conjugation Foundational AIMer SAR AIMers detected in liver of NHP at Day 50 (PK) ADAR editing with ACTB AIMer is highly specific ACTB Confidence (LOD score) % Editing RNA editing within full transcriptome (primary human hepatocytes) Substantial and durable editing in NHP liver in vivo (PD)  Day 50 RNA editing in NHP RNA editing only detected at editing site in ACTB transcript GalNAc AIMers GalNAc AIMers

Expanding addressable disease target space using AIMers to activate pathways and upregulate expression Modulate protein-protein interaction Upregulate expression Modify function Post-translational modification Alter folding or processing Restore or correct protein function Achieved POC WVE-006 (GalNAc AIMer) AATD POC: proof of concept Correct G-to-A driver mutations with AIMers Modulate protein interactions with AIMers AIMers provide dexterity, with applications beyond precise correction of genetic mutations, including upregulation of expression, modification of protein function, or alter protein stability

n=2; Primary hepatocytes 48h of treatment with the indicated dose concentration of AIMers  Modulation of protein-protein interactions: AIMers enable activation of gene pathway in vivo with single edit

Upregulation: AIMers can edit RNA motifs to restore or upregulate gene expression RNA binding proteins recognize sequence motifs to regulate various mRNA properties Enhance or inhibit mRNA decay Stability Intracellular localization Transport Splicing Capping Processing PolyA usage Translational efficiency Protein production mRNA AIMer edits mRNA à “dials up” gene expression A I(G) Decay No binding RNA binding protein Edited mRNA

AIMers upregulate mRNA and downstream serum protein in vivo above anticipated threshold In vitro to in vivo translation of mouse Target A mRNA upregulation In vivo mRNA upregulation corresponds to an upregulation of Target A protein in serum at Day 7 demonstrating proof-of-concept mRNA upregulation 7 days post-initial dose GalNAc AIMer Protein upregulation 7 days post-initial dose GalNAc AIMer Upregulation mRNA editing 7 days post-initial dose GalNAc AIMer Target A (undisclosed liver target) High unmet need with potential for multiple large indications Preserves endogenous protein function Serum protein with biomarkers of pathway activation Potential benefit 3-fold+ upregulation in mouse Potential threshold for benefit hADAR mouse dosed subcutaneously 3 x 10 mg/kg GalNAc-conjugated AIMer or PBS days (0, 2, 4), taken down at day 7 RNA editing

Wave’s discovery and drug development platform

Silencing Proprietary PN chemistry enhances potency across modalities Improved knockdown Splicing Improved skipping Ranked by potency of reference PS/PO compound Ranked by potency of reference PS/PO compound PS/PO reference compound PS/PN modified compound % Skipping Target knockdown (% remaining) Left: Experiment was performed in iPSC-derived neurons in vitro; target mRNA levels were monitored using qPCR against a control gene (HPRT1) using a linear model equivalent of the DDCt method; Middle: DMD patient-derived myoblasts treated with PS/PO or PS/PO/PN stereopure oligonucleotide under free-uptake conditions. Exon-skipping efficiency evaluated by qPCR. Right: Data from independent experiments RNA Editing Improved editing PS/PO/PN PS/PO (Stereopure) PS/PO (Stereorandom) Concentration (mM) % Editing

Potential for best-in-class RNAi enabled by Wave’s PRISM platform **** Left, Middle: Mice expressing human HSD17B13 transgene treated (3 mg/kg)siRNA or PBS, liver mRNA, guide strand concentration, Ago2 loading quantified. Stats: Two-way ANOVA with post-hoc test * P<0.05, ****P<0.0001. Liu et al., 2023 Nuc Acids Res doi: 10.1093/nar/gkad268; Right: ICV: Intracerebroventricular; APP: Amyloid precursor protein ; CNS: central nervous system; B6 mice were administered PBS or 100 μg of APP siRNA by ICV injection on day 0 (n=7). Mice euthanized 8 weeks after administration. Taqman qPCR assays used for RNA PD, relative fold changes of App to Sfrs9 mRNA normalized to percentage of PBS group. All treated group show P≤0.0001 compared to PBS group in 2way ANOVA. Wk 2 Wk 14 Wk 7 Reference Wave siRNA * * Ago2 loading (liver, transgenic mice) Wave siRNA Reference PBS Unprecedented Ago2 loading following administration of single subcutaneous dose RNAi is one of multiple Wave modalities being advanced in strategic research collaboration with GSK First in vivo study of unconjugated siRNAs demonstrated 70-90% APP silencing across six brain regions in mouse CNS at 8 weeks

WVE-006 for AATD Most advanced RNA editing candidate & potential best-in-class approach for AATD WVE-006 CTA submissions expected in 2H 2023 Expansion opportunities in liver, CNS and kidney Newest modality in Wave platform Preclinical data suggest best-in-class potential for Wave RNAi capability Hepatic, CNS and beyond Delivering on pipeline and platform catalysts RNA EDITING RNAi DISCOVERY PIPELINE & COLLABORATIONS Anticipate investor event in 3Q 2023 during which Wave will demonstrate how it is continuing to extend its leadership in RNA editing and share preclinical data on new wholly-owned programs Advance collaboration activities with GSK, with potential for additional cash inflows in 2023 and beyond WVE-N531 for DMD Potential best-in-class approach with highest exon skipping reported Dosing in potentially registrational clinical trial expected in 2023; data expected in 2024 Expansion opportunities in other exons, as well as other muscle diseases and CNS SPLICING WVE-003 for HD First-in-class wtHTT-sparing approach Data expected 2H 2023 WVE-004 for ALS/FTD Variant-selective approach for C9orf72 Data expected 1H 2023 Enables discussion on next steps with Takeda ANTISENSE SILENCING

Realizing a brighter future for people affected by genetic diseases For more information: Kate Rausch, Investor Relations InvestorRelations@wavelifesci.com 617.949.4827