This evidence explains why the over-activation of PKB/AKT caused by excessive production of the membrane lipid PIP3 (phosphatidyl-Inositol-3,4,5-tris-phosphate), produced by PI3K, is observed in 50% of human cancers [6,7,8], while defects in the PKB/AKT pathway is associated with metabolic diseases (diabetes and insulin resistance) [9]. This evidence concerns the gene AKT1 and Insulin resistance.