The suggestion has frequently been made that lipid-laden blood monocytes might contribute to atherosclerosis by emigrating into the arterial intima. In spite of much evidence that this occurs, the mechanism has never attracted widespread support as being of major importance, mainly because of the apparently small numbers of monocytes involved in this traffic, compared to the larger numbers of smooth muscle cells in the lesion. Recent observations suggest that some at least of the macrophages within the early lesion may be oxidising their lipid contents. Because some oxidised lipids are known to be toxic to cells, it is proposed that the production of oxidised lipids by macrophages may cause the death of these and other cells in the intima; and that-cell death begins the vicious circle of injury and further lipid accumulation which characterise the enlarging plaque.