MEK inhibitors such as selumetinib and trametinib have shown modest responses in relapsed or refractory RAS-mutated AML, although resistance often develops through compensatory activation of the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT)-mammalian target of rapamycin (mTOR) pathway [15,16]. Here, AKT1 is linked to acute myeloid leukemia.