Our short-read transcriptomic data reveals that multiple TCF4 exons (n = 5) were significantly dysregulated in Exp+ compared to control and Exp- FECD samples (Fig 3A and S12 and S13 Tables), whereas no significant differences were observed between Exp- and control (PWC3, Fig 3B and S12 and S13 Tables), demonstrating for the first time that differential TCF4 exon usage is driven by CTG18.1 expansions and not a downstream feature of FECD unrelated to the primary genetic driver. The gene discussed is TCF4; the disease is Fuchs endothelial corneal dystrophy.