[2] Studies of ex-vivo or cultured human corneal endothelium and mouse models of disease have reported evidence of apoptosis, [17], [18] endoplasmic reticulum stress, [19], [20] and oxidative stress. [21] However, some studies have focused upon cases or models of disease associated with minor genetic variants due to several known mutations unrelated to TCF4. Studies of oxidative stress in FECD have described a down-regulation of genes and proteins involved in antioxidant pathways, including nuclear factor erythroid 2-related factor 2 and multiple peroxiredoxins. [21], [22]. The gene discussed is TCF4; the disease is Fuchs' endothelial dystrophy.