First, our cellular and in vivo studies have shown that Vps35 is necessary for SLC4A11 cell surface targeting (Fig 5), and Vps35 deficiency caused a loss of SLC4A11 protein (Fig 5); Second, mutations in SLC4A11gene, which result in a loss of SLC4A11’s function [40, 45], have been identified in patients with three genetic corneal dystrophies, including CHED2, Harboyan syndrome, and FECD. This evidence concerns the gene SLC4A11 and congenital hereditary endothelial dystrophy of cornea.