While BL6 and FVB/N mice developed many metabolic defects with western diet feeding, the A/J mouse strain, which also developed NASH and F1 fibrosis, was completely refractory to diet-induced obesity and various metabolic defects, including hyperglycaemia and hyperinsulinemia, and exhibited only very mild glucose intolerance and even mild improvements in insulin sensitivity. The gene discussed is INS; the disease is hyperinsulinism.