Studies conducted with DcR3 transgenic mice with actin promoter-driven expression of human DcR3 demonstrated these mice to manifest a lupus-like syndrome after 5-6 months of age, thus, suggesting that DcR could play a role in the complex intertwinement of mechanism that drive the pathogenesis of lupus-like syndromes. This evidence concerns the gene TNFRSF6B and drug-induced lupus erythematosus.