The process of atherosclerosis always—100 percent of the time—starts with a penetration of the (damaged) artery wall by a rogue lipoprotein. Many things, such as high blood pressure or cigarette smoke, may weaken and damage that artery wall, making it an easy target for penetration. But it’s the LDL particle that “does the deed” and actually moves into that “no-parking” zone. It takes up residence, and thus begins the cascade of plaque formation that can lead to a lot more serious stuff.