New studies have demonstrated similarities in the complex pathomechanisms of diabetes mellitus type 1 (T₁D) and rheumatic diseases and in particular rheumatoid arthritis (RA). Common HLA gene complex characteristics and polymorphisms of inflammatory cytokines, such as interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) play a special role in both disorders. The metabolic syndrome, associated with insulin resistance and diabetes mellitus type 2 (T₂D), often shows criteria of a subclinical chronic inflammation. New forms of therapy with monoclonal antibodies against TNF-α, IL-1 and IL-6 have improved the management of patients with RA. Cytokine-induced inflammation also seems to be important in the pathogenesis and progression of T₁D and T₂D. Whether a therapy with the same monoclonal antibodies established in RA could also be successful in diabetes still has to be investigated in further studies. Both RA and T₁D are autoimmune disorders and show a cumulative incidence with further autoimmune diseases.