Further, the decreased serum levels of BCAAs that we observed in T2DM are in line with the results of Shin et al. [57] who demonstrated that alteration in hypothalamic insulin signaling can decrease plasma BCAA levels by inducing the hepatic activity of branched-chain α-keto acid dehydrogenase, a rate-limiting enzyme in the BCAA degradation pathway. The gene discussed is INS; the disease is type 2 diabetes mellitus.