Indeed, dimeric fusion proteins of the PLAD of TNFR1 with glutathione S-transferase or the Fc domain of human IgG1 have been successfully used in preclinical in vivo models to treat TNF/TNFR1-driven diseases, such as collagen- and CpG DNA-induced arthritis, skin lesion development in lupus-prone mice, spontaneous autoimmune diabetes, and myelin oligodendrocyte glycoprotein (MOG)-induced encephalomyelitis (Deng et al., 2005, 2010; Wang et al., 2011). This evidence concerns the gene TNFRSF1A and systemic lupus erythematosus.