As detailed in a comprehensive review of the research implicating CTG18.1 expansion in disease pathogenesis, the proposed mechanisms by which the CTG18.1 expansion may drive or exacerbate the onset of FECD include TCF4 dysregulation, toxic gain-of-function from TCF4 repeat-containing RNA, toxic gain-of-function from repeat-associated non-AUG-dependent translation, and somatic instability of CTG18.1 [41]. Here, TCF4 is linked to Fuchs endothelial corneal dystrophy.