These data are consistent with previous data demonstrating that APOC3 can cause inflammation in various cells, including endothelial cells,10 monocytes,29 and adipose tissue,11 and support the hypothesis that increased plasma levels of APOC3 may also make individuals more prone to develop NASH in addition to simple steatosis.9 However, the increased circulating cytokines were not associated with hepatic NF-κB p65, JNK phosphorylation, and ceramide content, indicating the hepatic inflammatory signals may not be the major factors for aggravating the hepatic insulin resistance in ApoC3Tg mice. Here, NFKB1 is linked to steatosis.