CDKN2A deletion causes sensitivity to palbociclib (Ramsey et al, 2007; Dean et al, 2010; Wiedemeyer et al, 2010; Young et al, 2014), therefore the CDKN2A mutation may explain why RPE1 cells arrest so efficiently in G1 following CDK4/6 inhibition (the IC50s for palbociclib and abemaciclib are comparable to the most sensitive cancer cell type in a panel of 560 tested lines: see Fig 1A and (Gong et al, 2017)). The gene discussed is CDK4; the disease is cancer.