Recent work from our laboratory using antigen‐specific immunotherapy in NOD mice showed significant protection of diabetes progression by CD4+ type‐1 regulatory (Tr1) populations with sustained upregulation of PD‐1, accompanied by bystander tolerance of islet‐specific glucose‐6‐phosphatase catalytic subunit‐related protein (IGRP)‐specific CD8+ T cells.5 This evidence concerns the gene CD8A and diabetes mellitus.