Corneal stromal edema and disrupted CEC arrangement21,22, pathological features concomitantly found in FECD and CHED patients15 and in the slc4a11−/− mouse model23, suggest that loss of SLC4A11 function underlies the pathology associated with SLC4A11 mutations. This evidence concerns the gene SLC4A11 and Fuchs endothelial corneal dystrophy.