Using a chronic-binge model, we showed that IL-10, an iNKT-derived inhibitory cytokine, may be responsible for the alcohol-induced suppression of NK cell functions in the liver, since IL-10 expression was obviously upregulated in ethanol-exposed hepatic iNKT cells (Figure 9), and the reduced number and functions of hepatic NK cells were restored to normal levels in IL-10−/− mice undergoing chronic-binge alcohol consumption, and liver steatosis and injury were attenuated compared with WT controls (Figure 10). The gene discussed is IL10; the disease is fatty liver disease.