of TNF, TAK1 has become a novel target for the treatment of TNF mediated diseases such as auto immune disease ( Rheumatoid Arthritis, lupus, IBD) but also other cytokine mediated disorders such as chronic pain and cancer. With the advent of novel selective TAK1 inhibitors, groups have explored the therapeutic potential of TAK1 targeted therapies. One group has shown that the selective TAK1 inhibitor, Takinib developed at Duke University attenuated rheumatoid arthritis like pathology in the CIA mouse model of human inflammatory arthritis. Furthermore, pharmacological inhibition of TAK1 has shown to reduce inflammatory cytokines in particular TNF. Humans mutations A rare mutation in TAK1 in humans has been reported. The mutation leads to gain of function, and hyper activation of TAK1 signaling pathways. Patients with gain of function mutations often present with craniofacial abnormalities. Interactions MAP3K7 has been shown to interact with: ASK1, CHUK, MAP2K6, TAB1, MAP3K7IP2, MAP3K7IP3, Mothers against decapentaplegic homolog 6, PPM1B, and TRAF6. References Further reading External links EC 2.7.11