Furthermore, in the intermediate cytogenetic patients with AML, levels of both Gal-3 and phosphorylated AKT (S473) were positively correlated with phosphorylated GSK3α/β expression, indicating a function for Gal-3 in AKT-mediated repression of GSK3 in AML cells [72] (Figure 4). This evidence concerns the gene GSK3A and acute myeloid leukemia.