To investigate the mechanisms whereby AA consumption induces hypercholesterolemia in mice, liver lysates were prepared and western blotting analysis was performed to assess the protein expression of mediators of cholesterol synthesis and metabolism (LDLR, HMGCR, PCSK9, ABCG5, ABCG8, ApoB, and SREBP2) (Figures 4A–H). The gene discussed is LDLR; the disease is familial hypercholesterolemia.