These pro-inflammatory mediators, which are transcriptionally regulated by the ubiquitous and inducible nuclear factor-κB (NF-κB), exert their pleiotropic autocrine effects via downstream activation of activator protein-1 (AP-1) and NF-κB itself, thereby contributing to myocardial inflammation, dilated cardiomyopathy, cardiac hypertrophy and heart failure (Gupta et al., 2008; Palomer et al., 2013a, ,b). The gene discussed is JUN; the disease is inflammatory response.