Vaccination of A2.1-transgenic NOD mice with these NPPEs seems to accelerate T1D development, increasing insulitis and triggering the expansion of S100-β–specific CTLs, probably due to the expansion of high-affinity S100-β–specific cytotoxic T cells, suggesting that the use of short HLA class I–restricted peptides to induce tolerance needs a careful evaluation of the target cytotoxic population to avoid its stimulation. Here, S100B is linked to type 1 diabetes mellitus.