These studies show that the expression of SHIP1 is reduced in a significant number of T-ALL patient samples, and indicate a loss of function of SHIP1 in T-ALL cells, which may have a functional role in the leukemogenesis of T-ALL by influencing different signaling pathways (PI3K/AKT, MAPK and PLC). This evidence concerns the gene AKT1 and acute lymphoblastic leukemia.