Pro-inflammatory EVs exacerbate disease progression by promoting oxidative stress, foam cell formation, and pro-inflammatory cytokine release, while anti-inflammatory EVs derived from mesenchymal stem cells or engineered sources can attenuate atherosclerosis by suppressing NF-κB signaling, enhancing M2 macrophage polarization, and improving endothelial repair. Here, NFKB1 is linked to atherosclerosis.