Researchers led by David Liu at the Broad Institute unveiled PERT — prime editing‑installed suppressor tRNAs — a strategy to convert an endogenous tRNA into a suppressor that can restore protein production across diverse nonsense mutations. The approach, reported in Nature, demonstrated rescue of protein function in cellular models and disease models for multiple lysosomal storage disorders and Hurler syndrome in mice. Separately, a complementary prime‑editing advance shows that engineered suppressor tRNAs can substantially boost prime editing efficiency and readthrough of premature stop codons, improving the potential for disease‑agnostic genome editing therapies. Both studies emphasize prime editing’s flexibility and the field’s focus on one‑time, broadly applicable genetic medicines. Investigators reported no detectable off‑target edits in the tested contexts and highlighted delivery, long‑term expression, and safety as next hurdles. The work signals a shift toward editing paradigms that aim for one therapeutic agent to address multiple genetic lesions.