In a mouse model prone to atherosclerosis, deletion of the PCSK9 gene, independent of LDLR, reduced the production of adhesion molecules and chemotactic factors from endothelial cells, such as ICAM-1, monocyte chemoattractant protein-1 (MCP-1), and monocyte chemoattractant protein-3 (MCP-3), which facilitate monocyte adhesion and penetration into vascular walls [116]. The gene discussed is CCL2; the disease is atherosclerosis.