Researchers from David Liu’s group at the Broad Institute published a new prime editing‑based strategy, PERT (prime editing‑installed suppressor tRNAs), that converts endogenous tRNAs into suppressor RNAs to read through premature stop codons across diverse genes. The approach restored protein production in human cell models of Batten, Tay‑Sachs and Niemann‑Pick diseases and showed efficacy in a mouse model of Hurler syndrome. PERT does not directly correct each nonsense mutation; instead it permanently engineers a tRNA that suppresses premature termination codons broadly, enabling a single therapeutic agent to address multiple genetic diseases with nonsense mutations. The Nature paper reported no detectable off‑target edits or cellular toxicity in initial studies. Authors pitched PERT as a potentially scalable, one‑agent approach to rescue a class of genetic disorders, accelerating routes to clinical translation while emphasizing the need for delivery solutions and longer‑term safety data.