To dissect whether and when INS-DRiP-derived peptide recognition is altered in the course of disease progression, we co-cultured dispersed HLA-A2+ human islets treated with IFNα (type I) or IFNɣ (type II) with an HLA-A2-specific CD8+ T cell clone, isolated from an individual with type 1 diabetes and directed against the N-terminal part of the INS-DRiP polypeptide (INS-DRiP1–9) [7] (Fig. 1a). This evidence concerns the gene CD8A and type 1 diabetes mellitus.