We illustrate the identified mechanisms of RAS/MAPK/MCL-1 crosstalk in Fig. 4h, with genomic RAS mutation or epigenetic MAPK activation activating downstream MAPK signaling and stabilizing MCL-1, which in turn sequesters BIM from BCL-2, facilitates AML survival and maintains mitochondrial respiration, supporting cell metabolic fitness. The gene discussed is BCL2L11; the disease is acute myeloid leukemia.