PPARα antagonism leading to body‐weight loss (6); PPARα activation in utero leading to impaired fertility (18, 51); peroxisomal fatty acid β‐oxidation inhibition leading to steatosis (36); PPARα activation leading to liver tumors (37) and pancreatic acinar tumors (166); hepatic steatosis from NR1I3 (CAR) suppression (58), nuclear factor erythroid 2–related factor 2/farnesoid X receptor (NRF2/FXR) activation (61), and glucocorticoid receptor activation (318). This evidence concerns the gene NR3C1 and fatty liver disease.