SLC4A4 and dental enamel hypoplasia: Functional relevance is supported by Slc4a4-null models, which develop severe enamel hypoplasia and hypomineralization even without systemic acidosis, and by ameloblast-like cell systems (HAT7) that demonstrate sodium-dependent basolateral-to-apical bicarbonate transport and cytosolic alkalinization when NBCe1 is engaged.