PTEN, also known as phosphatase and tensin homolog, is one of the most frequently mutated tumor suppressors in human cancer and acts as both a dual-specificity protein phosphatase and a lipid phosphatase, removing the phosphate in the D3 position of the inositol ring from phosphatidylinositol 3,4,5-trisphosphate. It is the first phosphatase identified as a tumor suppressor. It may be involved in almost all types of cancer, both solid tumors and hematological malignancies. PTEN negatively regulates intracellular levels of phosphatidylinositol-3,4,5-trisphosphate in cells by serving to counter-balance the effects of PI3 Kinase, which normally generate PtdIns(3,4,5)P3 and acts as a tumor suppressor by negative regulation of AKT/PKB signaling pathway via preventing localization of proteins with pleckstrin homology domains to the cell membrane. Recent results indicate that at least part of its role is to regulate the activity of the serine/threonine kinase AKT/PKB, and thus influence cell survival signaling.