It is reported that TGF-β1 treatment increases the expression of pro-inflammatory cytokines, including interleukin-1 (IL-1) and metalloproteinase-1 in synovial fibroblasts from rheumatoid arthritis and normal individuals [40], and IL-1 secretion by chondrocytes has shown to stimulate MMP13 expression and cartilage degradation in OA [41]. The gene discussed is TGFB1; the disease is rheumatoid arthritis.