In mouse models of AML and CML, CD44 targeting suppressed progression and induced differentiation by disrupting the interaction with the bone marrow niche [57], experimental evidence pointing towards apoptosis induction by caspase- or calpain-dependent pathways [58,59] and to inhibition of proliferation through stabilization of the cyclin-dependent kinase inhibitor p27, which resulted in increased association with the cyclinE-Cdk2 complex [58,60]. Here, CDK2 is linked to acute myeloid leukemia.