Researchers in David Liu’s lab at the Broad Institute described a prime editing strategy called PERT (prime editing‑installed suppressor tRNAs) that converts endogenous tRNAs into suppressor RNAs to read through premature stop codons across different genes. Published in Nature, the team demonstrated restoration of protein production in cell models of Batten, Tay‑Sachs and Niemann‑Pick C1 disease, plus symptom alleviation in a mouse model of Hurler syndrome, without detectable off‑target DNA edits. PERT does not edit the disease-causing nonsense mutation directly; instead it permanently programs the translational machinery to bypass premature termination, creating a potentially disease‑agnostic one‑time therapeutic. The work, led by postdocs Sarah Pierce and Steven Erwood, sets a framework for broader, lower‑cost development paths for multiple rare genetic disorders and raises questions for regulatory assessment of editing‑installed cellular functions.