Changes in colony formation, the cell cycle distribution, and apoptotic rates caused by CPVL knockdown were reversed by adding SF1760 to MCF7‐R and ZR75‐1‐R cells incubated with palbociclib or ribociclib (Figure 3d–f,i–k and Supporting Information Figure S2), therefore SF1760 blocked CPVL and promoted resistance to CDK4/6 inhibitors by inhibiting PTEN activity in breast cancer. The gene discussed is CDK4; the disease is breast carcinoma.