The current hypothesis is that lung injury is not associated with direct virus-induced injury but that COVID-19 invasion triggers immune and inflammatory responses that lead to the activation of immune cells (macrophages, T and B lymphocytes, granulocytes, and monocytes) to release numerous pro- and anti-inflammatory cytokines, including TNF-α, IL-1β, and IL-6, and markedly increased levels of inflammatory markers, such as C-reactive protein and the erythrocyte sedimentation rate [74]. The gene discussed is CRP; the disease is COVID-19.