Diabetes studies have indicated that: (a) IL6 is normally expressed in islet beta and alpha cells, but its production is reduced in the pancreas of diabetics [37]; (b) elevated levels of IL-18 are found in the blood cells of T1D patients and may promote NK cell activation and abrogation of the suppressive capacity of T regulatory cells [38]; and (c) peripheral blood mononuclear cells of children who developed beta-cell autoimmunity have upregulated IL32 transcripts before the appearance of T1D-associated autoantibodies [39]. Here, IL32 is linked to diabetes mellitus.