Consistent with the corneal endothelium’s role as a pump, ion transport is a major theme of FECD genetics, most famously in the association of highly penetrant rare mutations in solute transporter SLC4A11. Our analysis also replicated the GWAS locus at ATP1B1, whose gene product regulates sodium balance as a subunit of a Na+/K+ ATPase. Here, ATP1B1 is linked to Fuchs endothelial corneal dystrophy.