Although the molecular mechanisms leading to processing and presentation of these ‘junk’ polypeptides remain unclear, the presence of insulin-derived defective ribosomal product (INS-DRiP)-specific CD8 T cells, with an effector phenotype in donors with type 1 diabetes, supports their potential relevance as autoimmune T cell targets [6, 7]. This evidence concerns the gene CD8A and type 1 diabetes mellitus.