In AML, insulin-like growth factor (IGF)-1 and its same-named receptor IFG-R1 significantly contribute to leukemogenesis, according to evidence that IGF-1/IGF-1R signaling exerts pro-leukemic effects on AML cells in vitro via activation of downstream PI3K/Akt and the extracellular signal-regulated kinase (Erk) pathways [144,145]. This evidence concerns the gene IGF1R and acute myeloid leukemia.