We hypothesized that high CKS1B expression in AML may provide a selective susceptibility to inhibition of either CDK-CKS1-dependent phosphorylation or SCF-CKS1-dependent protein degradation (SCFSKP2-CKS1 E3 ligase inhibitor, hereafter referred to as CKS1i)(26, 27). This evidence concerns the gene CKS1B and acute myeloid leukemia.