The lesions of atherosclerosis represent a protective, inflammatory-fibroproliferative response against the different agents that can cause the disease. If the injury continues chronically over a sufficiently long period of time, and if opportunity is not given for restitution of normal architecture in the artery wall, lesions may progress to a point at which clinical sequelae develop. On the other hand, as demonstrated by Brown et al, Kane et al, and Blankenhorn et al, the advanced lesions of atherosclerosis can be shown to regress. A quantitative, statistical analysis of angiograms in patients who are aggressively treated with lipid-lowering agents, such as HMGCoA reductase inhibitors has clearly shown this to be the case. Thus, it is entirely conceivable that this chronic, excessive, inflammatory, and fibroproliferative response can be reversed, given sufficient opportunity for the factors that have led to the endothelial and arterial wall injury causing these events to be taken into hand and modified.