Cardiovascular diseases (CVD) are the leading cause of death worldwide with 17 millions deaths every year and represent a major public health challenge. Atherosclerosis is the main cause of CVD characterized by the accumulation of lipids and leukocytes in the lumen of arteries and causing their narrowing and dysfunction. Despite current therapeutic interventions, the incidence of CVD is expected to markedly progress imposing an enormous burden on the health care systems. It is now well recognized that the state of chronic low-grade inflammation favor the onset and progression of CVD but the underlying mechanism is still poorly understood. Leukocyte counts, and monocytes in particular, have been shown to independently predict risk for CVD. Indeed, recruitment of inflammatory Ly6Chi monocytes in early vascular injury give rise to plaque macrophages and supply therefore the growth of the plaque. In line with these observations, circulating monocyte levels correlate with the degree of disease severity in humans and mice, and targeting C-C motif chemokine receptor 2 (CCR2)-dependent monocyte plaque infiltration prevents the development of atherosclerosis. Although extensive research has focused on elucidating the role of cytokines and the microenvironment in the migration and infiltration of monocytes, the cellular metabolic pathways that regulate these processes are not well understood. Therefore, there is a considerable therapeutic interest in better understanding the mechanisms linking monocyte metabolism to CV risks.