As for the responsible mechanisms, it has been proposed that overexpression of SOCS3 decreased IRS-1 and IRS-2 tyrosine phosphorylation [36], promoted IRS protein degradation [37, 38], and inhibited PI3K/Akt pathway [18, 19], thus leading to IR and consequently causing T2DM. This evidence concerns the gene AKT1 and type 2 diabetes mellitus.