Hepatocytes in patients with atherosclerosis inevitably suffer from mitochondrial dysfunction, immune status alteration, and necrosis, which induces liver inflammation, as seen by the overproduction of inflammatory factors including C-reactive protein (CRP), tumor necrosis factor- (TNF-) α, and leukocyte inflammatory chemical factors such as IL-6, IL-12, and monocyte chemoattractant protein-1 (MCP-1) [12]. This evidence concerns the gene CRP and atherosclerosis.