Although not clear explanation can be attributed to this phenomenon, however, the possible underlying reason can be the direct effects of pro-inflammatory cytokines in the Hashimoto’s thyroiditis against insulin resistance and deteriorating the pancreas’ β-cell function; TSH is a potent stimulator of interleukin (IL)-6, IL-2, C-reactive protein (CRP) and tumor necrosis factor (TNF)-α secretion from adipose tissue in patients with Hashimoto’s thyroiditis [36]. This evidence concerns the gene IL2 and Hashimoto thyroiditis.