comprehensively reviewed the essential contributions of RNA splicing to cardiac development and disease processes [10], noting that aberrant exon skipping in Titin, as observed in individuals with dilated cardiomyopathy (DCM), results in the production of a larger N2BA‐G isoform that compromises myocardial contractility and accelerates HF progression. Here, TTN is linked to familial dilated cardiomyopathy.