When the body is stimulated by bacterial infection or bacteria or aseptic inflammatory stimuli such as atherosclerosis and cerebral infarction, CRP binds to lipoproteins, the complement system is activated, many inflammatory mediators are produced, and oxygen free radicals are released, causing damage to the vascular intima and increased vascular permeability and aggravating the systemic inflammatory response. This evidence concerns the gene CRP and bacterial infectious disease.