The idea that over‐expression of typical pro‐inflammatory mediators such as the cytokines IL‐1B, TNFα, and IL‐6, as we found in the absence of iASPP, leads to DCM is in accordance with established data showing that the presence of these mediators in plasma, as well as in the myocardium itself, potentiates cardiac remodeling processes such as hypertrophy, ventricular dilation, fibrosis, and apoptosis (Gullestad et al, 2012; Dick & Epelman, 2016; Prabhu & Frangogiannis, 2016). The gene discussed is IL1B; the disease is familial dilated cardiomyopathy.