TNF-α can alsointensify myocardial inflammatory responses by activating the P38mitogen-activated protein kinase (MAPK) signaling pathway and upregulating theexpression of other proinflammatory factors, such as IL-1β [37, 38].Indeed, IL-1β is highly expressed in myocarditis and cooperates withTNF-α to promote neutrophil infiltration and NADPH oxidase activation,further amplifying inflammatory signals and inducing cardiomyocyte apoptosis[39]. The gene discussed is IL1B; the disease is myocarditis.