These dual degraders halt AML cell proliferation and induce myeloid differentiation via CK1α-p53 and IKZF2-dependent mechanisms, with their effectiveness confirmed in both AML cell transplanted mice models and cells form patients.311 Subsequently, PROTACs were developed that co-degrade CK1α and CDK7/9, stabilizing p53 and suppressing MYC, MCL-1, and MDM2. This evidence concerns the gene MDM2 and acute myeloid leukemia.