FLT3 mutations, common in AML-M2 and M4, activate PI3K/AKT and STAT5 pathways, driving cytokine production (tumor necrosis factor-alpha (TNF-α), IL-1β, IL-6, and granulocyte-macrophage colony-stimulating factor (GM-CSF)) and contributing to EN as a paraneoplastic phenomenon. This evidence concerns the gene AKT1 and acute myeloid leukemia.