PTPN11 and acute myeloid leukemia: The reduced sensitivity to venetoclax in RAS- and PTPN11-mutated AML patients can be explained by the activation of the RAS/MAPK signaling pathway [96], allowing the AML cells in RAS- and PTPN11-mutated cases to use multiple sources of energy for cell survival, including fatty acid and amino acid metabolism, glycolysis and upregulation of OXPHOS [97,98].