Through that lens, one could imagine the inflated population we have observed to be a polyclonal pool of effectors, some “autoreactive.” Such an expansion could explain the precipitous decline in beta cells that has been observed in the progression to diagnosed diabetes (95), as well as the negative association among CMV-specific CD8 T cells and c-peptide levels among diagnosed type 1 diabetics (96). Here, CD8A is linked to diabetes mellitus.