The type I interferon induced Cxcl9 that develops early in NOD has the ability to recruit both pathogenic and regulatory T cells that bear the Cxcr3, the receptor for Cxcl9. It is possible that the naïve T cell is incapable of being diabetogenic until it has been converted to an effector/memory phenotype at distal sites, such as the pancreatic lymph node, a site which has been shown important in diabetes development [33], [34]. This evidence concerns the gene CXCR3 and diabetes mellitus.