MAP2K7 and acute myeloid leukemia: However, the frequent development of resistance to kinase inhibitors, such as imatinib and sorafenib, through a variety of mechanisms such as acquisition of additional mutations within the kinase domains of the target proteins, leads us to an important question: will MEK inhibitor utility in AML be limited by rapid selection and expansion of subclones that either express or develop intrinsically resistant mutations in the pathway or that lack dependence on MEK signaling for growth and survival?