Although the established liver steatosis AOP has revealed that upregulation of CAR and PXR triggers KEs that ultimately result in hepatic lipid accumulation (Mellor et al. 2015; Vinken 2015), the interplay between these receptors is complex and varies depending on specific ligands and cellular context, which could explain the exhibited steatotic effect from the formulated product-equivalent mixture (1:1) and the formulated product. The gene discussed is NR1I3; the disease is fatty liver disease.