Taken together, the high prevalence of FECD in DM1 patients, the cosegregation of the disease phenotypes, the lack of TCF4 repeat expansion, and the robust expression of the DMPK gene in the corneal endothelium (Fig. 2), are compatible with a hypothesis that the DMPK gene may cause the FECD phenotype in some but not all patients with DM1. Here, TCF4 is linked to Fuchs endothelial corneal dystrophy.