Mice engineered to express mono- or biallelic A144E variants of tnrsf13B, corresponding to A181E, exhibited a striking resistance to pathogenicity and transmission of Citrobacter rodentium, a murine pathogen that models enterohemorrhagic Escherichiacoli, and resistance was principally owed to natural IgA deficiency in the intestine. This evidence concerns the gene CD79A and hyperinsulinemic hypoglycemia, familial, 4.