One of the key characteristics of molecular signaling mechanisms underlying metabolic insulin resistance in the clinical setting is selective impairment in PI3K/Akt signaling pathways while other major branches of insulin signaling including Ras/MAPK (ERK1/2, p38MAPK and JNK) pathways remain intact or are even enhanced30, 31, 32, 33. This evidence concerns the gene AKT1 and Insulin resistance.