Truncating mutations in TTN are the most well known, and exon skipping in patient‐specific cardiomyocytes derived from induced pluripotent stem cells could be rescued, preventing defective myofibril assembly and stability.54 Also, exon skipping prevented the development of DCM and improved contractile performance in TTN‐mutated mice.54 Gene replacement is a promising therapy for specific severe forms of genetic DCM when a mutation results in a low level or absence of the corresponding protein, which is mostly seen in pediatric cases of DCM. Here, TTN is linked to familial dilated cardiomyopathy.