Two academic teams published complementary advances aimed at broadening prime editing’s therapeutic reach. David Liu’s Broad Institute group reported a strategy (PERT) that uses prime editing to convert an endogenous tRNA into a suppressor tRNA, enabling a single editing agent to rescue diverse nonsense mutations across multiple genes. The work was detailed in Nature and showcased recovery in cell models and a mouse disease model. A separate Nature paper described boosting prime editing efficacy by installing suppressor tRNAs and engineering editing systems to increase readthrough of premature stop codons. Together, the studies present a disease-agnostic approach: rather than editing each pathogenic allele directly, they equip cells with a persistent translational bypass mechanism that restores full-length protein across multiple targets. Both teams reported extensive off-target and safety assessments; reviewers flagged translational and delivery challenges ahead of clinical translation. For developers, these papers signal new routes to one-to-many genetic therapies that could compress R&D timelines if delivery and regulatory hurdles can be solved.