David Liu’s Broad Institute team published a prime-editing approach called PERT that permanently converts an endogenous tRNA into a suppressor tRNA, enabling one editing agent to rescue diverse nonsense mutations across different genes. The method restored protein production in human cell models of Batten, Tay‑Sachs and Niemann‑Pick C1, and improved phenotypes in a mouse model of Hurler syndrome, with no detected off-target edits reported in the paper in Nature. A companion Nature study showed prime-editing can install suppressor tRNAs and highlighted advances that increase editing efficiency and safety. The groups reported no detectable toxicity and emphasized PERT’s potential to sidestep the need to design a separate therapeutic for each nonsense mutation, which account for a large share of pathogenic alleles. Clarification: prime editing is a CRISPR-derived method that writes specific DNA changes without making double-strand breaks, enabling precision edits in genomic DNA. These papers position prime editing as a platform capable of broad, disease-agnostic interventions rather than single-gene fixes.