The cellular uptake of exogenous PtdIns(3,4)P2 improved cell survival in 3AC treated leukemia cells in a dose-dependent manner, indicating that SHIP1 can also support growth of hematopoietic cancers through increased PtdIns(3,4)P2 and downstream AKT activation [115]. Here, AKT1 is linked to hematopoietic and lymphoid cell neoplasm.