Given the dramatic reduction in IL-4 expression in CD1d−/− livers, this may suggest that iNKTs contribute some but not all of the IL-4 protein in the liver under basal conditions, leading to a mild version of the phenotype observed by Ricardo-Gonzalez et al. This phenotype does not appear to be connected to either the steatosis or glucose intolerance observed in our model, as these were iNKT-independent. The gene discussed is IL4; the disease is steatosis.