The tumor-like proliferation of RASFs is considered to be the major mechanism for the hyperplasic growth of the RA synovium and eventual destruction of the articular bones and cartilage.3 IL-1β plays an important role in the pathogenesis of inflammatory synovitis and joint destruction in RA by inducing the proliferation of fibroblast cell lines [13]. This evidence concerns the gene IL1B and rheumatoid arthritis.