Other work has demonstrated that a consequence of prolonged UPR activation resulting from chemically induced ER stress in mice compromised by genetic inactivation of either of various components of the UPR, is transcriptional suppression of metabolic gene expression networks in the liver leading to hepatic steatosis, at least partially through the inhibition of C/EBP-α by CHOP [33,34]. Here, DDIT3 is linked to fatty liver disease.