AKT1 and acute myeloid leukemia: This is due to hypoxia-induced cell cycle arrest and pro-survival signaling, as indicated by the upregulation of p27 (a regulator of cell cycle which prevents S-phase entrance), the increased expression of XIAP (an anti-apoptotic molecule), and the pro-survival PI3K/AKT pathway activation observed in AML cells upon in vitro culture in hypoxic conditions [76].