In line, Cxcl14 expression was enhanced in mouse primary macrophages by oxidized LDL, and peptide immune therapy diminished serum CXCL14 levels and murine atherosclerosis.49 Although attributed to macrophages so far, conditional deletion of Cxcl14 using existing Pdgfra- or future Dpep1-Cre models may unveil the effect of CXCL14+ fibroblasts in atherogenesis. This evidence concerns the gene CXCL14 and atherosclerosis.