It has also been shown that, in at least some primary AML cells, there is continued phosphorylation of ERK, STAT5, or AKT following inhibition of FLT3-ITD, which may contribute to the limited efficacy of FLT3 inhibitors used as single agents for the treatment of mutant FLT3-positive AML [32]. Here, AKT1 is linked to acute myeloid leukemia.