Recently, using a combination of NGS and dideoxy sequencing, Herman et al. [9] estimated TTN truncating variants (TTNtv)—nonsense, frameshift and essential splice site, to be responsible for approximately 25% of familial cases of idiopathic dilated cardiomyopathy (DCM) and 18% of sporadic cases in a large cohort of subjects. This evidence concerns the gene TTN and familial dilated cardiomyopathy.