In obesity and hyperinsulinemia secondary to insulin resistance, there is a decrease in total testosterone related to lower SHBG levels resulting from either decreased hepatic synthesis of this protein [40] or a decrease in free testosterone to levels, which implies a real decline in testosterone production [9, 40, 41] in which Leydig cell steroidogenesis is impaired because of target organ resistance to insulin action and/or production of cytokines/hormones by the adipose tissue [35, 42]. The gene discussed is INS; the disease is hyperinsulinism.