This manifests as a decline in muscle function and structure, which could be attributed to an imbalance in protein synthesis and breakdown related signaling pathway like mammalian target of rapamycin (mTOR) [8], transforming growth factor-β (TGFβ) [9], etc. Disruptions in lipid metabolism related signaling, such as peroxisome proliferator-activated receptors (PPARs) [10], affect the fatty acid β-oxidation in muscles, contributing to the pathogenesis of Type 2 diabetes and metabolic syndrome [11]. The gene discussed is MTOR; the disease is type 2 diabetes mellitus.