Genotype-phenotype correlations can be best explained by phenotypic plasticity where mutations/variations in the same gene and even the same mutation/variation in a different background cause disparate phenotypes.[10] In the case of cardiomyopathies, such phenotypic plasticity was best illustrated by Dr. Seidman’s group, who reported that mutations in the MYH7 and TNNT2, encoding beta-myosin heavy chain and cardiac troponin T, respectively, could cause either HCM or DCM, the opposite ends of the spectrum of phenotypic responses of the heart to injury, stress or mutations.[11]. This evidence concerns the gene TNNT2 and familial dilated cardiomyopathy.