Researchers at the Broad Institute published a prime‑editing strategy that converts endogenous tRNAs into suppressor RNAs (PERT), enabling a single editing agent to rescue premature termination codons across multiple genes. David Liu’s team reported recovery of protein production in cell and animal disease models including Batten and Hurler syndromes. Related work in Nature detailed prime‑editing–installed suppressor tRNAs and improvements to prime editing using suppressor tRNAs, expanding the toolkit for disease‑agnostic genome correction. The studies reported restored protein function without detectable off‑target edits or overt toxicity in model systems. The approach aims to simplify genetic medicines by using one engineered editing event to enable readthrough of nonsense mutations across diverse loci. Translational steps will focus on delivery, long‑term expression, safety and regulatory pathways for a broadly applicable gene‑writing therapeutic.