The pathogenesis of T2DM involves intricate signaling pathways, including the impairment of insulin receptor substrates (IRSs)/phosphatidylinositol-3-kinase (PI3K)/Akt/glucose transporter 4 (GLUT4) signaling, which leads to reduced GLUT4 translocation; dysfunction of the AMP-activated protein kinase (AMPK) pathway, which disrupts glucose and lipid metabolism; and activation of inflammatory signaling pathways [2,4]. The gene discussed is SLC2A4; the disease is type 2 diabetes mellitus.