CDK4/6 and other CDKs and cyclins are often overexpressed in tumor cells, and activating mutations in CDK4 are oncogenic.2–10 CDK4 and CDK6 classically exert their effects on the cell cycle by phosphorylating retinoblastoma (RB) protein, enabling the release of the E2F transcription factor, resulting in the transcription of genes required for subsequent cell cycle events, such as cyclins E and A.2 However, data demonstrate that CDK4/6-regulated cell cycle activation also occurs through the inhibition of TGF-β signaling.11 Here, CDK4 is linked to neoplasm.