It is well characterized that overproduction and overexpression of TNF-α acts as a key initiator in the inflammatory cascade, activating members of the Interleukin-family such as Interlekuin-1β (IL-1β), enhancing interactions between T-and B-lymphocytes, synovial-like fibroblasts and macrophages, leading to synovial inflammation and joint destruction [3, 53]. The gene discussed is IL1B; the disease is inflammatory response.