There is an autocrine stimulatory loop by interaction between TIM-3 and Gal-9 in AML cells that contributes to AML development and leukemic cell survival through phosphorylation of extracellular signal-regulated kinase (ERK), activation of protein kinase B (PKB, also known as AKT) and induction of the β-catenin pathway and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) [15–17]. This evidence concerns the gene AKT1 and acute myeloid leukemia.