Consequently, TIGIT-deficient mice are more prone to EAE due to a hyperproliferative T-cell response, while TIGIT overexpression on CD4+ T cells in a mouse model of RA alleviates disease severity, supporting the inhibitory function of TIGIT and its role in the regulation of autoimmune responses through the TIGIT/DNAM-1 axis [29,65,99,100]. The gene discussed is CD226; the disease is rheumatoid arthritis.