It is now well-established that CYP-derived EETs have potent anti-inflammatory effects in preclinical models of NF-κB-mediated vascular inflammation [12], [38], and also exhibit anti-apoptotic and anti-fibrotic properties [15], [39], [40]; therefore, the observed suppression of hepatic EET biosynthesis may propagate the inflammatory response and thus be detrimental in the pathological progression of NAFLD/NASH. This evidence concerns the gene NFKB1 and metabolic dysfunction-associated steatotic liver disease.