The major limitation of our work is the small number of patients and the restricting panel of analyzed genes, particularly the noninclusion of titin that accounts for up to 20–25% of all DCM cases [27], as well as other “arrhythmogenic” genes (when the study was designed, the panel of genes was chosen, given the published overall percentage of dilated cardiomyopathy cases caused by pathogenic variants in each gene, being one of the broader panels available at the time for cardiomyopathies). The gene discussed is TTN; the disease is dilated cardiomyopathy.