The observation that the intestinal chloride–bicarbonate exchanger and the sodium–hydrogen exchanger protein-3 protein—which are mutated in CCD and CSD, respectively—are regulated by MYO5B (but not CTE- or THES-associated genes) and were mislocalized in the postnatal MVID intestine [16,17] suggests that the fetal bowel abnormalities in MVID and in CCD/CSD may share the same etiology. Here, MYO5B is linked to microvillus inclusion disease.