The hallmark of COVID-19 pathogenesis is the excessive activity of immune cells, such as macrophages and T helper 1 cells (Th1), with the consequent release of pro-inflammatory cytokines, including interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, and IL-8, that exacerbate the inflammatory response and mediate alveolar and endothelial damage [4,5]. This evidence concerns the gene TNF and COVID-19.