However, the question arises, whether the reduced numbers of inflammatory cytokine secreting T cells in the csDMARD treated patients constitute some kind of protection from inflammageing associated cardiovascular disease [50], cognitive impairment [33, 51] and additional autoimmune manifestations in RA, or whether the increased numbers of IFNγ+CD8+ cytotoxic T cells and Th17 cells in the TNFi treated patients renders them less prone to experience severe viral infections than RA patients with other treatment regimens [52]. The gene discussed is CD8A; the disease is viral infectious disease.