Although it is not possible to exclude the possibility that alternative osteoblastic factors downstream of mTORC1, such as Cxcl1 and Ccl2, could be involved in the development of AML, communication between osteoblasts and AML cells within the BM microenvironment plays a crucial role in AML progression, at least in part, through mTORC1-IL-6 axis in osteoblasts and IL-6R-JAK/STAT3 axis in AML cells. Here, CCL2 is linked to acute myeloid leukemia.