This included a reduced number or efficacy of diabetogenic splenocytes, a lower number of circulating CD8+ T cells reacting to both insulin and IGRP, increased resistance of islet grafts to autoimmune destruction, and significantly lower islet infiltration both in spontaneous diabetes development and in chimeras reconstituted with G9C8 bone marrow (shown in reference 22). Here, G6PC2 is linked to diabetes mellitus.