CYP7A1 and metabolic dysfunction-associated steatotic liver disease: N-IgY combined with omega-3 polyunsaturated fatty acids led to significant upregulation of genes involved in cholesterol uptake (LDLR), reverse cholesterol transport (ABCG5/ABCG8), and BA metabolism (CYP7A1), representing a promising treatment strategy to prevent HFD-induced MASLD through the activation of cholesterol catabolism to BAs and by decreasing cholesterol-induced fibrosis [103].