The higher disease activity in the MetS+ RA patients might be due to a common molecular background shared by both RA and MetS: the release of inflammatory cytokines such as tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6), which lead to synovial inflammatory infiltrates from one side to an impaired metabolic profile from the other side [37]. The gene discussed is TNF; the disease is metabolic syndrome.