KAT7 and Werner syndrome: Beyond cancer, a genome-wide CRISPR-based screenidentified KAT7 as a driver of cellular senescence in two types of humanmesenchymal precursor cells (hMPCs) with pathogenic mutations found inaccelerated aging diseases such as Werner syndrome and Hutchinson-Gilfordprogeria syndrome[256].Inactivation of KAT7 decreased histone H3K14ac and decreased p15INK4bexpression, thereby delaying senescence in hMPCs.