Together these data suggest that loss of water movement capacity contributes to the corneal dystrophies and hearing defects in people with defective SLC4A11. Fluid accumulation in the corneal stroma arises from processes that either increase water accumulation in the stroma or decrease water reabsorption into the aqueous humour, which is accomplished by the corneal endothelial cell layer. This evidence concerns the gene SLC4A11 and corneal dystrophy.