Fig. S4B) between control and EC-ACKR3-deficient mice, circulating CXCL12 levels correlated significantly with atherosclerotic lesions sizes in the control mice, whereas this correlation was lost in the absence of endothelial ACKR3, suggesting that ACKR3–CXCL12 interactions drive atherosclerosis (Fig. 1O). The gene discussed is CXCL12; the disease is atherosclerosis.