Given that other viral and bacterial infections are established triggers for disease relapses, it is plausible that the hyperinflammatory state induced by COVID-19—characterized by elevated levels of pro-inflammatory cytokines such as IL-6, IL-1β, and TNF-α—might exacerbate endothelial dysfunction and enhance vascular permeability [21]. The gene discussed is IL6; the disease is endothelial dysfunction.