In progerin-expressing mice, the progeroid phenotype can be ameliorated and lifespan increased by CRISPR-Cas937,38 and base-editing approaches36 to ubiquitously correct the HGPS-causing mutation or by the delivery of antisense oligonucleotides to block pathogenic splicing of mutant lamin A transcripts14,39,40; however, these treatments were administered to asymptomatic neonates and young animals. The gene discussed is LMNA; the disease is Hutchinson-Gilford progeria syndrome.