This landmark discovery of a common genomic variant shed light on the pathology of FECD, and subsequent research based on this discovery proposed the following hypothetical mechanisms underlying FECD: (1) dysregulated expression of TCF4 transcripts; (2) toxicity of the TNR primary RNA transcripts; (3) repeat-associated non-AUG translation; and (4) TNR length instability.16 This evidence concerns the gene TCF4 and Fuchs endothelial corneal dystrophy.