A-FABP deficiency generates a lipid environment that is highly favorable for insulin action: mice lacking A-FABP had altered lipid composition in muscular tissue (upregulation of shorter chain [12:0 and 14:0] fatty acids, and downregulation of longer chain [16:0 and 18:0] fatty acids), leading to an upregulation in insulin-stimulated phosphorylation of Akt and protecting against high-fat-induced insulin resistance, thus enhancing the insulin signaling cascade [84]. The gene discussed is INS; the disease is Insulin resistance.