However, we failed to detect any difference in the expression of proinflammatory mediators between non-obese and obese OA patients, suggesting that the chronic low grade of inflammation associated with obesity rather than the OA-related joint inflammation is involved in the overexpression of TGFβ, IGF-1 and TIMP-2 in both chondrocytes and adipocytes. The gene discussed is TGFB1; the disease is obesity due to melanocortin 4 receptor deficiency.