These observations suggest that G-to-A transition is a characteristic mutation under MSH2 deficiency, and that induction of this base substitution in Ctnnb1 is a key event in tumorigenesis [31] in the small intestine of Msh2-KO mice, but the induction of mutations other than G-to-A transition was expected to enhance tumorigenesis by administration of potassium bromate because the administration of this agent did not cause any further increase in the frequencies of G-to-A transition. This evidence concerns the gene CTNNB1 and hyperinsulinemic hypoglycemia, familial, 4.