Although most experts in the field of T1D autoimmunity pathogenesis agree that insulin and GAD65 are the major T1D auto-antigens, and therefore, by adding peptides from these proteins at the time of tDC generation could provide some level of antigen-specificity in terms of what populations of autoreactive T-cells are suppressed, the same experts note that by the time of disease onset, a significant degree of antigen spreading has occurred where other “late-antigen”-specific T-cells may in fact be driving autoimmunity. This evidence concerns the gene INS and type 1 diabetes mellitus.