In this study, we revealed that the NR REV-ERBα serves as a key link between the dietary CLA-induced hepatic steatosis and the downregulation of the circadian gene program in the liver, while another NR PPARα serves as the major CLA respondent and facilitates the REV-ERBα-mediated transcription repression of the circadian genes and its recruitment of histone repressors in the CLA-treated mice. Here, NR1D1 is linked to fatty liver disease.