Subsequent ACE2-mediated neutrophil infiltration, as well as NET formation, might be responsible for the exaggerated inflammatory response, which in turn contributes to the development of cardiovascular diseases, e.g., thrombosis, atherosclerosis, and endothelial injury, etc. One in five hospitalized COVID-19 patients showed increased troponin, brain natriuretic peptide, lymphopenia, and inflammation markers, such as c-reactive protein, IL-1β, and IL-6 in the early course of the disease suggesting cardiac injury [49,50]. The gene discussed is IL1B; the disease is COVID-19.