The immunopathophysiological basis of TAO has been further demonstrated, particularly by the study of mechanisms such as T-cell-mediated immune injury, IL-33 release, MyD88-dependent TLR signaling pathway, inflammation in the sympathetic ganglia, and inhibition of collateral artery development through IFN-γ and vascular endothelial growth factor receptor 1 (VEGFR1) (Sharebiani et al., 2020). The gene discussed is IFNG; the disease is thromboangiitis obliterans.