The contribution of adaptive immunity to NASH is further supported by the observations that steatosis, parenchymal injury, and lobular inflammation are lowered in immunocompromised Rag1−/− mice, lacking mature B-, and T-cells [12] as well as following the selective ablation of B-lymphocytes or CD8+ T-cells [36,37]. The gene discussed is CD8A; the disease is metabolic dysfunction-associated steatohepatitis.