Despite the ability of sEHIs to attenuate inflammation in the previous NAFLD models [40,42,43], AUDA and genetic sEH deletion had limited ability to attenuate LPS-induced hepatic pro-inflammatory cytokine production (IL6, iNOS, TNFα) in the early phase of inflammation following LPS insult. This evidence concerns the gene EPHX2 and metabolic dysfunction-associated steatotic liver disease.