Because both Met and Dex can down-regulate expression of several inflammatory genes involved in the pathogenesis of RA, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-68, we hypothesized that RA treatment with a combination of Met and Dex could effectively inhibit the pathogenesis of RA and induce cartilage regeneration in vivo. This evidence concerns the gene IL1B and rheumatoid arthritis.