Recruitment of circulating monocytes to the arterial intima contributes to the formation of atherosclerotic lesions and may participate in their destabilization. Leukocyte emigration from blood into tissues is mediated by multiple adhesion molecules and chemokines, which orchestrate specific steps of emigration and regulate preferential recruitment of different leukocytes depending on their expression patterns of chemokine receptors. Over the last several years, a number of adhesion molecules, including VCAM-1, P-selectin and ICAM-1, the chemokines MCP-1 (also known as CCL2) and IL-8 (also known as CXCL8), and their respective receptors CCR2 and CXCR2, have been functionally implicated in atherosclerosis. Two studies—one recently published in the JCI (1), and the second reported in this issue (2)—expand this list to include the chemokine receptor CX3CR1, the receptor for fractalkine (also known as CX3CL1).