To explore the crucial mechanisms involved in the selenoneine-mediated reversion to hepatocellular injury and hepatic steatosis, changes in the mRNA levels of pro-inflammatory cytokine genes (tumor necrosis factor α (Tnfα), interleukin-1β (Il-1β), and interleukin-6 (Il-6)) and oxidative stress-related genes (heme oxygenase 1 (Hmox1), glutathione S-transferase alpha 1 (Gsta1), and glutathione S-transferase alpha 2 (Gsta2)) were analyzed (Table 2). The gene discussed is GSTA2; the disease is fatty liver disease.