As FLT3 plays a criticalrole in AML pathogenesis, targeting FLT3 signalling represents a promising therapeutic strategy for the development of novel drugs.PLX3397 can be an indirect FLT3 inhibitor, and there has been some research interest in its potential application in acute myeloidleukemia (AML) because of its ability to target the tumor microenvironment by inhibiting CSF1R, which is involved in the regulation ofmacrophages and other immune cells within the bone marrow [17]. Here, CSF1R is linked to acute myeloid leukemia.