Several studies have shown that RORγt, IL-17A, IL-6, IL-22, and IL-23 levels are significantly increased in PBMCs of AIH patients.32–36 Wu et al37 found that IL-17A expression was significantly elevated in both AIH patients and Con A-induced AIH mice and that T-cell-immunoglobulin and mucin domain 3 (Tim-3) may inhibit Th17 cell-related expression and AIH through the p38-MKP-1 pathway. The gene discussed is IL22; the disease is autoimmune hepatitis.