Patients with FH display increased lipid accumulation in circulating monocytes.21,22 In mouse models, lipid-laden circulating monocytes showed upregulation in CD11c and an increased potential to invade nascent atherosclerotic lesions.23 Several studies in humans align with these findings, for example, a postprandial increase in monocyte lipid droplets associated with proinflammatory features of the same cells.57 The gene discussed is ITGAX; the disease is familial hyperaldosteronism.