Protein-truncating variants in constitutive exons (Percent Spliced In>90%) of TTN and in DSP were significantly enriched in patients with DCM compared with healthy controls (TTN 11.3% DCM vs 0.4% healthy controls, P=6.2×10−27; DSP 1.4% vs 0.0%, P=4.2×10−3). The gene discussed is DSP; the disease is familial dilated cardiomyopathy.