The development of insulin resistance (IR) occurs at a molecular level when there is an imbalance between excessive nutrients or inflammatory cytokines and the cell membrane receptors(Lonardo et al. 2015; Boden 2011), which IRS1 phosphorylation at serine307 and sequentially results in compromised ability of IRS1 to combine with insulin receptors and then decreases Akt phosphorylation at serine473, and then resulted in the inhibited potency of insulin signal transduction. The gene discussed is IRS1; the disease is Insulin resistance.