Researchers at the University of Texas Southwestern demonstrated targeted base‑editing strategies that corrected LMNA point mutations in patient‑derived iPSC cardiomyocytes and humanized mouse models, preventing cardiac pathology and extending lifespan in treated animals. The team optimized guide RNAs and CRISPR base editors to reverse disease phenotypes associated with R249Q and L35P mutations, normalized contractile and calcium handling defects in vitro, and suppressed arrhythmias in vivo. Results published in PNAS highlight base editing as a potential therapeutic route for laminopathies and provide preclinical data supporting further translational development.