Several pro-inflammatory molecules can variably participate to the cytokine storm driving ARDS in COVID-19, as demonstrated by different clinical studies reporting higher circulating levels of one or more immunoactive molecules in patients with severe form of COVID-19, including IL-1β, IL-2, IL-6, IL-7, IL-8, IL-17, TNF-α, IFN-γ, granulocyte-macrophage colony-stimulating factor (GM-CSF), CXCL10, CCL2, CCL7, CCL3, CCL4, and C-reactive protein (CRP) (209, 214–220). This evidence concerns the gene TNF and COVID-19.