In more severe COVID-19 cases, however, elevated and steady exhaustion levels and reduced functional diversity of T-cells in peripheral blood together with higher production levels of type 2 (IL-5, IL-9, IL-10, and IL-13) and type 3 (IL-17A/F and IL-22) responses have been found, suggesting that this later promotes the activation of the production of proinflammatory cytokines, including IL-1β, IL-6, CXCL8/IL-8, TNF, and CXCL10/IP-10, also associated with neutrophils and lymphoid organ damage (blocking T-cell response) (61, 64, 65), in severe COVID-19 patients. The gene discussed is IL17A; the disease is COVID-19.