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]. The gene discussed is MTOR; the disease is acute myeloid leukemia.