Pro-inflammatory cytokines such as IL-1 and tumor necrosis factor alpha (TNFα), which are potent stimuli for the p38 MAPK pathway, are elevated in the infarcted heart and appear to be detrimental for post-MI myocardial remodeling and progression to heart failure (Aukrust et al., 2005). The gene discussed is TNF; the disease is myocardial infarction.