AKT1 and neoplasm: It also has a multifunctional profile and has been shown to cause caspase-dependent apoptosis of tumor cell lines [12,13], inhibit bFGF and tumor induced neovascularization in vivo [14,15], abrogate AKT/PKB phosphorylation required for endothelial cell migration[14] and tumor cell proliferation[16],, inhibit proangiogenic TNF-α production[17], and activate and stimulate proliferation of cytotoxic T-cell lymphocytes[18].