For instance, genetic disruption of β-arrestin1 (Li et al., 2013), IFT20 (Yuan et al., 2014), and CD80/86 (O'Neill et al., 2007) suppresses arthritis development by impairing T cell differentiation and activation, while loss of NFAT5 (Choi et al., 2017), IKKβ (Armaka et al., 2018), CIKS (Pisitkun et al., 2010), and SIRT1 (Woo et al., 2016) inhibits arthritis pathogenesis by promoting apoptosis in macrophages and fibroblasts, or inhibiting antibody production and dendritic cell maturation, respectively. This evidence concerns the gene CD80 and arthritic joint disease.