The mechanisms underlying the onset of cardiomyopathy in, e.g., RBM20 deficiency involve incorrect processing of several splicing targets at once, including important contractile and structural proteins, such as calcium/calmodulin-dependent protein kinase II delta (CaMKIId), ryanodine receptor, tropomyosin, troponin, and titin, thereby affecting the structural and functional properties of cardiomyocytes including calcium handling [20], [21], [22]. Here, TTN is linked to cardiomyopathy.