In an immunocompetent mouse model of AML, OBs were significantly inhibited by a factor secreted by the leukemic cells, suggested to be the chemokine CCL3, that was also confirmed to be increased in the BM of primary patient samples of AML.(29) Additionally, during a murine model of myeloproliferative neoplasia, MSCs differentiated into functionally‐altered osteoblastic lineage cells due to signals from leukemic myeloid cells that include TPO and CCL3, among other local paracrine signals, driving the expansion of the osteoblastic lineage cells. This evidence concerns the gene TPO and acute myeloid leukemia.