Although it does not perfectly mimic all pathophysiological processes of rheumatoid arthritis, but is a widely used, well-defined and internationally accepted model with several similarities in the mechanisms (T cell dominant immune response with increase of TNFα, IL-1β, IFNγ, IL-6, IL-17 levels) and symptoms (synovial hyperplasia, inflammatory cell accumulation, cartilage destruction and bone erosion) of the human disease. The gene discussed is IFNG; the disease is rheumatoid arthritis.