Considering that iASPP interacts and represses transcriptional activity of NF‐κB (Yang et al, 1999; Takada et al, 2002; Herron et al, 2005; Sullivan & Lu, 2007) and that dysregulation of NF‐κB is involved in the development of heart failure (Gordon et al, 2011), we hypothesized that absence of iASPP can unleash NF‐κB to increase transcription of pro‐inflammatory mediators and, as a consequence, induce prolonged inflammatory processes and eventually DCM. The gene discussed is NFKB1; the disease is heart failure.