CCL3 and acute myeloid leukemia: Moreover, the secretion by LSCs of a bone morphogenic protein (BMP), of a negative regulator of osteogenesis (DKK), and of a chemokine that decreases osteocalcin and switches MSC differentiation from adipogenic to osteoblastic with the consequent accumulation of progenitor and immature osteoblasts and defects in bone mineralization (CCL3, also known as MIP1α) [33,34], contribute to creating a milieu of facilitating leukemia cell growth and AML progression.