Serum levels of SARS-CoV-2 viral elements and/or DAMPs released by host-infected and necrotic cells detected in COVID-19 patients may also activate the TLR4 pathway via the myeloid differentiation factor 88 (MyD88)-dependent pathway, which, resulting in an amplified proinflammatory response, may also have a role in SARS-CoV-2-induced myocarditis [23,106,111,112,113]. The gene discussed is TLR4; the disease is myocarditis.