In mouse models of atherosclerosis using both transgenic models expressing human CRP, or knockout models of endogenous CRP, CRP has been differently reported to (1) accelerate progression of atherosclerosis in apo E-deficient mice (69); (2) slow the development of atherosclerosis (70, 71); and (3) have no effect (72). The gene discussed is APOE; the disease is atherosclerosis.