CDK2 implicated in blocking differentiation of AML cells,418 is challenging to target specifically due to highly similar ATP-binding sites with other CDKs.419 Rao’s group designed a potent and selective CDK2-targeting PROTAC CPS2, promoting cellular differentiation by degrading CDK2 in various myeloid/lymphoid cell lines without obvious toxicity.420 Moreover, Cheng et al. developed an orally available triple-target CDK 2/4/6 degrader, demonstrating potent degradation and effective induction of apoptosis in various cancer cells, particularly in malignant melanoma.421. The gene discussed is CDK2; the disease is acute myeloid leukemia.