More important, impairment of Akt plasma membrane translocation resulted in inhibition of its activation, as indicated by our subsequent studies showing that exogenously added InsP5 inhibited phosphorylation of Akt in ovarian cancer line SKOV-3 cells [62], in PTEN-/- embryonic stem cells [62], in human umbilical vein endothelial cells (HUVEC) activated with basic fibroblast growth factor (FGF-2) [63] and in dissected tumours from a xenograft model of SKOV-3 cells [63]. The gene discussed is FGF2; the disease is neoplasm.