There are no data regarding the frequency or avidity of S100-β–specific CD8+ T cells in the A2.1-transgenic NOD mice; hence, we speculate that a combination of low affinity for MHC molecules and a quick peptide clearance from the injection site leads to the expansion of high-avidity CD8+ T cells, explaining the acceleration of T1D in vaccinated animals and the simultaneous increase in cytotoxicity against targets preincubated with S100-β NPPEs. The gene discussed is CD8A; the disease is type 1 diabetes mellitus.