Additionally, blocking IL-36R or IL-36α, both found to be elevated in inflamed knee joints of TNF-induced arthritic mice compared to wild-type controls, had no effect on clinical onset, pattern of disease or histological evidence of arthritis suggesting that IL-36 cytokines do not affect the development of inflammatory arthritis in vivo [229], potentially due to redundancy with other members of the IL-1 family such as IL-1, a dominant cytokine in rodent arthritis models [226]. The gene discussed is IL36A; the disease is arthritic joint disease.