The canonical signalling pathway promotes p65/p50 NF‐κB dimers, and the non‐canonical signalling promotes RelB/p52 dimers.51 TNF‐α activates the canonical NF‐κB signalling pathway.50 A previous study indicated that p50−/−mice were resistant to TNF‐α–induced cardiomyopathy and had enhanced cardiac function after myocardial infarction.52, 53 Therefore, targeting NF‐κB responses are essential for the development novel therapeutic interventions for heart failure following myocardial injury. The gene discussed is RELB; the disease is cardiomyopathy.