Recent studies have shown that for many DPs, DCM can be attributed to either 1) a splice site deletion in the pyruvate dehydrogenase kinase 4 (PDK4) gene, 2) a missense variant in the titin (TTN) gene, or 3) an unfortunate combination of both mutations in the same dog6,8. This evidence concerns the gene PDK4 and familial dilated cardiomyopathy.