The main possible mechanisms underlying this phenomenon are as follows: (a) IL-2 and IFN-γ may participate in the thyroid autoimmune process and affect thyroid function (Krieg et al., 2018) by blocking the PD-1/PD-L1 pathway; (b) IFN-γ and TNF-α produced by Th1 cells induce the release of CXCL10 from thyroid cells. The gene discussed is TNF; the disease is thyroiditis.