TG2−/− mice have impaired glucose-stimulated insulin secretion and show glucose intolerance after intraperitoneal glucose loading.158 The TG2−/− mouse phenotype resembles that of maturity-onset diabetes in young patients who have several missense mutations located near the catalytic site of TG2 and impaired transamidation activity.158, 159 However, TG2-disrupted mice and the constitutive transamidation active form of TG2-expressing mice show no significant differences in responses to a glucose or insulin challenge, suggesting that glucose homeostasis is TG2 independent.160. The gene discussed is INS; the disease is Glucose intolerance.