AKT1 and Insulin resistance: Phosphorylation of membrane phosphoinositide 2 (PIP2) to phosphoinositide 3 (PIP3) by PI3K starts Akt/PKB activation.10,11 Defects in phosphorylation of the insulin receptor and its substrates, and non-activation of PI3K-Akt/PKB has an important role in developing insulin resistance.10,12 If not activated, the Akt/PKB pathway will also not phosphorylate its substrates, which participate in various cell functions, such as control of metabolism, survival, glucose uptake, proliferation, growth and angiogenesis.13