This could be due to additional inhibition of CDK2 by alvocidib, as activation of the CDK2‐cyclin E pathway has been proposed as one of the resistance mechanisms to CDK4/6 inhibition [63] and targeting CDK2 in addition to CDK4/6 overcame resistance to CDK4/6 inhibitors in breast cancer [64, 65]. The gene discussed is CDK4; the disease is breast cancer.