To address this concern in the mVEGF-A KO system, we performed clodronate liposome macrophage depletion, followed by intravenous injection of cultured BMDMs that were polarized toward an inflammatory state with LPS + IFN-γ to confirm that macrophages are sufficient to rescue the myeloid VEGF-A-deletion phenotype in the experimental PAD model. This evidence concerns the gene IFNG and peripheral arterial disease.