Several autoimmune disease models have been shown to be dependent on posttranslational modifications of relevant Ags (e.g. on acetylation of a myelin basic protein peptide (MBP-Ac1-11) [40] or on the isoaspartyl-modification of a self Ag in a mouse model of systemic lupus erythematosus [41] or of peptides in DR4-transgenic mice expressing human type II collagen [42]. The gene discussed is TNFRSF10A; the disease is autoimmune disease.