Type B insulin resistance is characterized by autoantibodies to the insulin receptor, inducing severe insulin resistance requiring administration of suprapharmacologic doses of exogenous insulin for treatment. A case report by Declue, Shah, Marchese and Malone (1) described a young woman who carried a presumptive diagnosis of ovarian hyperthecosis and was subsequently found to have type B insulin resistance. However, once she was treated with antibody depletion therapy and circulating insulin levels normalized, the serum testosterone level normalized, indicating that the presumed diagnosis of hyperthecosis was incorrect. We present the case of a 49 year old African American woman who developed type B insulin resistance at the age of 45, requiring upwards of 1800 units of insulin daily. Simultaneously, she developed oligomenorrhea; excessive hair growth on the chin, chest, upper abdomen and upper thighs; and biochemical androgen excess with a serum total testosterone level of 275 ng/dL. At the age of 46, the type B insulin resistance was treated with two infusions of rituximab, dexamethasone, and cyclophosphamide. Her insulin requirements dropped precipitously, to the point where she currently requires only oral metformin; her current HbA1c is 6.1%. Her serum testosterone level, however, has remained elevated at 67 ng/dL, indicating a persistent hyperandrogenic state. Symptoms of a postmenopausal state were confirmed by a highly elevated serum FSH level of 44.1 mIu/mL; she is presently amenorrheic. A transvaginal ultrasound revealed a right ovarian volume of 19.3 mL and a left ovarian volume of 12.4 mL; 3 anechoic follicles were noted on the left, the largest of which measured 14.5 x 14.0 x 15.0 mm; 2 anechoic follicles were noted on the right, the largest of which measured 18.9 x 21.5 x 16.8 mm; bilateral hydrosalpinges were identified. A CT scan of the adrenals was normal. A presumptive diagnosis of hyperthecosis has been made, and the patient has been referred for bilateral oophorectomy. We postulate that, in this patient, the exposure of the ovaries to extremely high circulating insulin resulted in stimulation of the ovarian thecal cells and, ultimately, in autonomous function, yielding a clinical state of hyperthecosis. Reference: (1) Brown RJ, Joseph J, Cochran E, Gewert C, Semple R, Gorden P. Type B Insulin Resistance Masquerading as Ovarian Hyperthecosis. J Clin Endocrinol Metab. 2016;102(6):1789-1791.