Both studies in mouse models and meta-analyses of human genetic data indeed have linked immunoproteasome subunit deficiency (in mice) and specific polymorphisms in the immunoproteasome subunit genes LMP2/β1i and LMP7/β5i (in humans) to different, in part CD8+ T-cell-mediated autoimmune syndromes such as T1D. This evidence concerns the gene CD8A and type 1 diabetes mellitus.