In the recent years, atherogenesis has increasingly been linked to inflammatory processes in the injured vessel wall. Recruitment and arrest of monocytes, T cells, and neutrophils via the concerted actions of multiple chemokines and their chemokine receptors have been the subject of intense research and are being appreciated as key events underlying atherosclerotic lesion formation and progression. The evolutionary conserved cytokine macrophage migration inhibitory factor (MIF) exhibits prominent proinflammatory and proatherogenic functions, and the latest findings on its chemotactic and chemokine-like properties imply MIF as a crucial drug target for the treatment of inflammatory diseases. In this review, the role of MIF in atherosclerosis and injury-induced neointima formation is discussed. We place an emphasis on its proinflammatory and chemokine-like functions in the context of underlying extra- and intracellular signaling mechanisms. These findings clearly distinguish MIF from other cytokines in atherosclerosis and justify the intensive search for inhibitors targeting MIF in the treatment of inflammatory diseases, including advanced atherosclerosis.