Since SLC4A11 is induced by oxidative stress, reduced NRF2 expression may explain presence of oxidative stress in CHED patients due to diminished or total loss of SLC4A11 functions owing to mutations of SLC4A11. Although there is significant reduction of a few antioxidant genes in CHED patients, we found that is not the case for NQO1 which suggest that there might be some redundant mechanism of NQO1 regulation involving other transcription factors45. Here, SLC4A11 is linked to congenital hereditary endothelial dystrophy of cornea.