Capitalizing on these new molecular insights and the in vivo results establishing the causal role of TXNDC5 in atherogenesis, we devised a targeted nanomedicine platform that integrates PEI nanoparticles and CRISPR-Cas9 plasmids with an endothelium-specific promoter (human CDH5) (30), which specifically deleted Txndc5 in the endothelium and, moreover, significantly reduced atherosclerosis in ApoE−/− mice. This evidence concerns the gene APOE and atherosclerosis.