In AML, IL1RAP physically interacts with and mediates signaling through FLT3 and c-KIT, two receptor tyrosine kinases that induce JAK2/STAT phosphorylation and AKT and MAPK activation in response to the FLT3 ligand (FLT3L) and stem cell factor (SCF), respectively, thereby increasing proliferation, invasion, and migration [49]. The gene discussed is FLT3; the disease is acute myeloid leukemia.