A recent study [10] by Moretti, Gramlich (co-authors on this manuscript) and co-workers using AuP iPSC-CM demonstrated that: (1) Correction of TTN reading frame in patient-specific cardiomyocytes derived from induced pluripotent stem cells rescued defective myofibril assembly and stability and normalized the sarcomeric protein expression (2) AON treatment in TTN knock-in mice improved sarcomere formation and contractile performance in homozygous embryos and prevented the development of the DCM phenotype in heterozygous animals. This evidence concerns the gene TTN and familial dilated cardiomyopathy.