Researchers in David Liu’s lab at the Broad Institute described a prime‑editing strategy—termed PERT—that installs suppressor tRNAs via prime editing to rescue premature termination codons across multiple genes. The approach, published in Nature, restores protein expression in cell models of several lysosomal and neurodegenerative disorders and improved symptoms in a mouse model. PERT converts an endogenous tRNA into a suppressor RNA that reads through nonsense mutations without editing the underlying pathogenic allele; authors report no detected off‑target edits or toxicity in their preclinical work. The method could allow a single editing agent to address many distinct genetic diseases that share nonsense mutations as a mechanism. Broad investigators and observers see PERT as a potentially efficient, disease‑agnostic route for one‑time genetic medicines, though translational hurdles—delivery, durability and regulatory paths—remain to be addressed.