Specifically, we observed that in atherosclerosis-prone ApoE knockout animals, LAV-BPIFB4 gene transfer causes a CXCR4-dependent redistribution of the two major monocyte subsets with increased circulating Ly6Chigh cells and reduced Ly6Clow subsets, a protective macrophage polarization toward the pro-resolving M2 phenotype, and a reduction in T-cell activation23. The gene discussed is BPIFB4; the disease is atherosclerosis.