Thin filament HCM is most associated with mutations in TNNI3 and TNNT2 and may present with “non-classic” findings, including apical hypertrophy, higher risk of SCD, restrictive phenotype, and lesser degrees of left ventricular hypertrophy and LV outflow tract obstruction than that observed with thick filament mutations (5, 9, 33–37). This evidence concerns the gene TNNT2 and Schnyder corneal dystrophy.