Preclinical evaluation of JAK-STAT inhibition (such as JAK inhibitors: ruxolitinib, lestaurtinib, pacritinib, etc.)had demonstrated that this treatment strategy could inhibit AML cell proliferation; however, in some early-stage clinical trials, patients with single-agent JAK inhibitors could not achieve a promising therapy response, and this might be due to the crosstalk of JAK-STAT signaling pathway and other oncogenic pathways in the AML (31). Here, SOAT1 is linked to acute myeloid leukemia.