TCF4 and Fuchs endothelial corneal dystrophy: Conversely, as the occurrence of FECD is largely associated with an intronic CTG repeat expansion in TCF4, the utilization of gene-silencing technology, such as antisense oligonucleotides, to target the TCF4 TNR expansions within FECD primary CEnCs to suppress the expression of these CTG repeats to mitigate RNA toxicity has been described [41], thereby opening a plausible gene-based strategy for FECD treatment.