Going into our analysis, one plausible hypothesis was that tumors with high levels of Rb phosphorylation prior to treatment might be more sensitive to CDK4/6 inhibition; demonstrating the opposite suggests that, in these cancers, CDK4/6 inhibitors do not sufficiently block Rb phosphorylation to promote binding of the E2F transcription factor and impede cell cycle progression. This evidence concerns the gene RB1 and cancer.