A missense mutation in human MCT8 has been reported, leading to consistently elevated T3 levels and partially recapitulates a hyperthyroidism phenotype including persistent tachycardia, which reduces to a normal heart rate with treatment.[29] We can then speculate that over-expression of MCT8, present in myocardium of SCD mice, may modify opposing effects with a phenotype similar to hypothyroidism, with further exacerbation of diastolic blood pressures and function in the myocardium as is evident in a subset of patients with SCD. This evidence concerns the gene SLC16A2 and Schnyder corneal dystrophy.