Deletion of ACKR3/CXCR7 in apoE−/− mice results in increased atherosclerotic lesion formation and the application of a small molecule ACK3 agonist decreases atherosclerosis by a mechanism that relates to the expression of ACK3 in white adipose tissue, where it takes part in cholesterol metabolism (Li et al., 2014). Here, APOE is linked to atherosclerosis.