These mice differed from RGS2−/− mice in that they had severe hyperglycemia, glucose intolerance, hypoinsulinemia, reduced islet insulin content, and glucose-stimulated insulin release.18 It is also worth noting that the impact of Gαs deletion on β-cell mass and proliferation was observed at birth, but only later in RGS2−/− mice, suggesting distinct functions of RGS2 and Gsα in pancreatic β cells. The gene discussed is GNAS; the disease is Glucose intolerance.