Of note, its mutation in patients causes a severe form of familial dilated cardiomyopathy.72 CircRNA profiling by RNA‐seq of human hearts allowed the identification of 80 circRNAs originating from the titin gene (TTN), a gene that is known to undergo highly complex alternative splicing.73 A subset of these circRNAs are dynamically regulated in dilated cardiomyopathy and RBM20‐null mice completely lack these titin circRNAs. The gene discussed is TTN; the disease is dilated cardiomyopathy.