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. The gene discussed is IFT20; the disease is arthritic joint disease.