For example, Duparc et al. recently reported that, in a rodent model, the hepatocyte specific deletion of Myd88 predisposes to inflammation, hepatic steatosis, and insulin resistance [59]; other reports suggested that the deletion of Myd88 increases the risk of developing features of metabolic syndrome such as diabetes and hepatic steatosis [60, 61]; conversely, deletion of MyD88 in intestinal epithelial cell-specific murine model partially protected against diet-induced obesity, diabetes, and metabolic inflammation [62]. This evidence concerns the gene MYD88 and Hepatic steatosis.