Furthermore, due to the higher CXCL12 secretion by AML BM-MSC or CXCR4 superexpression in LSC, the leukemic cells have a greater ability to modulate CXCL12/CXCR4 axis facilitating their trafficking and homing into the protective BM microenvironment, maintaining their quiescence and protected from chemotherapeutic compounds (Wang and Zhong, 2018). Here, CXCR4 is linked to acute myeloid leukemia.