For example, palbociclib-resistant breast cancer (MCF-7pR) cells that had undergone prolonged treatment with palbociclib acquired CCNE1 gene amplification and sustained high levels of CDK2 Thr160 phosphorylation, and the silencing of CCNE1 or CDK2 alone in these cells did not affect cell-cycle arrest. The gene discussed is CDK2; the disease is breast carcinoma.