In HT development, enhanced secretion of interferon (IFN)‐γ, interleukin (IL)‐1β, IL‐2, and tumor necrosis factor (TNF)‐α paralleled by thyroid cell apoptosis occurs due to the impaired T helper (Th)‐1‐based immune response, whereas in GD, upregulated production of IL‐4, IL‐5, IL‐6, and IL‐13, resulting from the Th2‐driven humoural response, causes the secretion of autoantibodies recognizing thyroid‐stimulating hormone receptor (anti‐TSHR) and hypertrophic changes.2 This evidence concerns the gene IL6 and hematocrit.