AKT1 and neoplasm: These include alteration of K+, Na+, Ca2+ homeostasis, inhibition of glycolysis, increased production of reactive oxygen species, inhibition of topoisomerase II, upregulation of death receptors, alteration in membrane fluidity, increased level of p21, inhibition of NF-κB signaling, inhibition of Akt activation, down regulation of interleukin 8 receptor, induction of tumor cell differentiation, inhibition of soluble fms-like tyrosine kinase, and loss of mitochondrial membrane potential [13, 34, 35].