In the present study, we have extended these previous studies by revealing that AZD1208 in combination with PI3K/Akt inhibitors not only inhibited proliferation but also induced apoptosis at least partly by reducing expression level of Mcl-1 downstream of mTORC1 pathway in FLT3-ITD-driven cells, including MV4-11, and that AZD1208 significantly enhanced the effects of GDC-0941 on viable cell numbers and Mcl-1 expression levels in some of primary AML cells expressing FLT3-ITD. Here, FLT3 is linked to acute myeloid leukemia.