Elevated circulating levels of pro-inflammatory peptides produced by mononuclear cells, observed in patients with AD, strongly suggest a role of a disturbed balance between pro-inflammatory cytokines, such as interleukin-1 (IL-1), interleukin-2 (IL-2), tumor necrosis factor alpha (TNF-α), and interferon-γ (IFN-γ), and those with anti-inflammatory properties, such as interleukin-4 (IL-4), interleukin-10 (IL-10), and tumor growth factor-β (TGF-β) in the pathogenesis of both types of autoimmune diabetes [4–6]. This evidence concerns the gene IL2 and Alzheimer disease.