As summarized in Table 5, of the 27 CNS proteins homologous to Tg, 2 (7%; nidogen-1/entactin and ephrin type-B receptor 2) were reported to generate autoAb, and in the following conditions: certain types of glomerulonephritis, autoimmune uveoretinitis, systemic lupus erythematosus and related disorders (systemic vasculitis, rheumatoid arthritis), pulmonary renal syndrome, the Aicardi-Goutières syndrome, acute necrotizing encephalopathy, and systemic sclerosis [52], [53], [54], [55], [56], [57], [58], [59], [60], [61], [62]. This evidence concerns the gene TG and necrotizing vasculitis.