PF4 and atherosclerosis: As a result, leukocyte β2 integrins macrophage antigen-1 (Mac-1) and lymphocyte function-associated antigen-1 (LFA-1) are activated and platelets produce chemokines, including platelet factor 4 (PF4), a vital mediator of atherosclerosis, to enhance the adhesion of monocytes, which will further turn into macrophages and will finally become foam cells by lipid uptake [11].