On the other hand, genetic ablation of A20 (Matmati et al., 2011), PGRN (Tang et al., 2011), and CTRP6 (Murayama et al., 2015) increased the susceptibility of mice to experimental arthritis development by promoting NF-κB activation, TNFα-mediated inflammation and complement activation, respectively. This evidence concerns the gene C1QTNF6 and arthritic joint disease.