In CD-fed LDLR−/− hamsters, expression of Fat-1 significantly elevated the anti-inflammatory mediators, including EPA-derived HEPE and DHA-derived MaR, while concurrently decreasing the AA-derived pro-inflammatory mediator hydroxyeicosatetraenoic acid, further supporting the beneficial impact of elevated HEPE on dyslipidemia, atherosclerosis, and MAFLD as previously reported in mice [37,38]. This evidence concerns the gene LDLR and atherosclerosis.