In summary, we conclude that BBR intervention for the ARD rats can suppress proinflammatory and profibrosis responses, improve redox status in the kidney, lower hypercholesterolemia, and eventually ameliorate renal injury, and that such effects appear to be mediated by inhibition of the activity of the NFκB signaling pathway. The gene discussed is NFKB1; the disease is familial hypercholesterolemia.