From humans and pre-clinical animal models, the role of fibrotic deposition in the myocardium (with its eventual impact on cardiac function) and the development of diastolic dysfunction have been previously observed.[2] Herein, we report that three genes, interleukin-18 (IL18), α-L-fucosidase A2 (FUCA2), and thyroid hormone transporter (SLC16A2), appear to be upregulated in SCD-associated diastolic dysfunction. This evidence concerns the gene FUCA2 and Schnyder corneal dystrophy.