Lack of disease-associated mutations within the coding regions of TCF4 reported by us and subsequently confirmed by Riazuddin et al. (Baratz et al., 2010; Riazuddin et al., 2011), raised the possibility that the genetic variant(s) underlying the FECD association could reside in a non-coding region of TCF4. Given the natural history of FECD as an autosomal dominant, late-onset genetic disease, we explored the possibility that variations in CTG18.1 repeat length could represent the underlying causal variant. The gene discussed is TCF4; the disease is hereditary disease.