Thus, the disruption of the IRS2 gene and the consequent dysregulated insulin secretion and hyperinsulinemia described in the male Irs2−/− mice joint to the increase in intracellular cAMP levels linked to a sexual dimorphism31, could underlie in proliferation of thyrocytes and other morphological findings observed in the present study in the thyroid follicles of those male IRS2-KO animals. The gene discussed is INS; the disease is Hyperinsulinemia.