First, the cholesterol hypothesis in atherosclerosis originates from the Anichkov rabbit model [21]; secondly, cholesterol feeding induces very high CRP levels in the plasma as well as CRP deposition in atherosclerotic plaques in the rabbit model [19]; and thirdly, complement C6 deficiency in rabbits protects these animals from lesion development [22, 23]. The gene discussed is CRP; the disease is atherosclerosis.