In fact, numerous pro-inflammatory stimuli, such as TNF-α, IL-1β, and oxidized lipoproteins, activate the endothelial inflammatory cascade via NF-κB (Maracle et al., 2018), while Su et al. observed that inhibiting TLR4/MyD88/NF-κB signaling with nicorandil ameliorated lipopolysaccharide (LPS)-induced myocardial inflammation and improved cardiomyocyte survival (Su et al., 2018). This evidence concerns the gene NFKB1 and myocarditis.