However, the above-mentioned hypothesis has three conflicting points: (i) mitochondrial biogenesis can occur simultaneously to insulin resistance, (ii) disruption of mitochondrial function leads to increases in basal and insulin-stimulated glucose uptake in some models, and (iii) most studies actually show that fat oxidation is increased in obese, insulin-resistant individuals and T2DM patients. The gene discussed is INS; the disease is Insulin resistance.