Evidence shows that the immune system is implicated in developing or progressing TAO via the oxidative stress, T cell-related immune injury, IL-33 release, MyD88-dependent TLR signaling pathway, sympathetic ganglia inflammation, COX inflammatory pathway, impaired development of collateral arteries by IFN-γ and VEGFR1, and HMGB 1. The gene discussed is MYD88; the disease is thromboangiitis obliterans.