Researchers in David Liu’s laboratory reported a prime-editing strategy called PERT (prime editing–installed suppressor tRNAs) that converts an endogenous tRNA into a suppressor RNA to read through premature termination codons across multiple genes. The Nature report demonstrated restored protein production in human cell models of Batten, Tay–Sachs and Niemann–Pick disease, and therapeutic benefit in a mouse model of Hurler syndrome without detectable off-target edits or toxicity. PERT reframes prime editing from target-by-target correction to a disease-agnostic suppressor approach that could reduce the need to develop a separate editing drug for each nonsense mutation. The team highlighted the potential efficiency gains for rare-disease development but noted further work is needed on delivery, long-term expression and regulatory pathways before clinical translation.