Once recruited in the site of infection, neutrophils release different proinflammatory mediators, including cytokines (interferon-α, interferon-β, tumor necrosis factor, and interleukins 1β, 6, and 10) and chemokine (e.g., CXCL10) that participate in COVID-19 pathogenesis [102]. This evidence concerns the gene CXCL10 and infection.