Accumulation of classical monocytes is imperative for the progression ofatherosclerosis. Hence, therapeutic interference with mechanisms oflesional monocyte recruitment, the primary mechanism controllingmacrophage accumulation, may allow for targeting atheroprogression andits clinical complications. Here, we review the important role ofclassical monocytes in atheroprogression as well as their routes ofarterial recruitment. We specifically highlight the role of celladhesion molecules as well as of platelet-derived chemokines andneutrophil-borne alarmins.