For example, an increase of thrombin activity in patients with dilated cardiomyopathy [154,155] can contribute to the fragmentation of cTnT, which can have both pathogenetic significance (damage to cTnT, which is one of the main components of the contractile apparatus of cardiomyocytes), and diagnostic value: a decrease in the size of the cTnT molecule as a result of fragmentation, and a possible increase in the release of these fragments into the bloodstream. This evidence concerns the gene TNNT2 and dilated cardiomyopathy.