Heterozygous changes in SLC4A11 have been reported in cases of late onset Fuchs endothelial corneal dystrophy (FECD; OMIM 136800) in which haploinsufficiency and accumulation of aberrantly folded protein is reported to result in FECD pathology [15]. Here, SLC4A11 is linked to Fuchs endothelial corneal dystrophy.