In males, consistent with impaired hepatic insulin sensitivity, deletion of hepatic Rictor resulted in fasting and glucose-stimulated hyperinsulinemia, and increased HOMA2-IR, despite negligible effects on the response to an ITT (Figure 5E, Figure 5—figure supplements 1–2); castration did not have a significant effect on any of these parameters. The gene discussed is INS; the disease is hyperinsulinism.