Although these data also show that there are other pathophysiological mechanisms of FLD that do not involve UPR activation, our recent report that overexpression of active Atf6 in hepatocytes is sufficient to cause steatosis in zebrafish larvae (Howarth et al., 2014) demonstrates that this key UPR player is probably an important mediator of this disease in some instances. This evidence concerns the gene ATF6 and steatosis.