In patientswith dysfunctional insulin receptors, including type B IR or insulin receptor mutations,it is not clear how insulin signals within the ovary to increase androgen productionbecause one would expect all pathways downstream of the insulin receptor to be blocked.Furthermore, in rodents, selective insulin receptor deletion in theca cells preventshyperandrogenism induced by hyperinsulinemia (8);however, germline insulin receptor mutations in humans do result in hyperandrogenism(9). The gene discussed is INSR; the disease is Hyperinsulinemia.