Studies have found that neutrophils induce endothelial cells to express monocyte chemoattractant protein-1 and intercellular adhesion molecule-1 by releasing NETs, which aggregate macrophages and promote atherosclerotic lesions.[77] Megens et al[75,78] found that NETs activate the autoimmunity of plasmacytoid dendritic cells (pDCs) in atherosclerotic lesions, cause a large amount of IFN-I synthesis and release, and then strengthen the inflammatory response to promote the progression of AS. The gene discussed is CCL2; the disease is Atherosclerotic lesion.