Moreover, FFA also activates c‐Jun amino‐terminal kinase and protein kinase C (PKC), stimulates insulin receptor substrate‐1 (IRS1) phosphorylation, and inhibits phosphatidylinositol‐4,5‐bisphosphate 3‐kinase and Akt activation, resulting in a reduction in glucose transporter type 4 (GLUT4) expression (Kim, 2012), indicating that lipid accumulation is a factor in the creation of IR and hyperglycemia. This evidence concerns the gene SLC2A4 and Hyperglycemia.