In the physiopathology of acute myocarditis, inflammation plays a key role characterized by the activation of nuclear factor κB (NF-κB) signaling pathways and the release of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukins (IL): IL-1, IL-6, IL-12, and IL-23 [2,9]. The gene discussed is TNF; the disease is acute myocarditis.