Considering the growing evidence of the key role of CRP as an inflammatory mediator involved in the development of atherosclerosis and endothelial dysfunction, it is expected that CRP may be more powerful in triggering the pro-inflammatory function of CD32-expressing cell subsets such as platelets, endothelial cells, monocytes, and leukocytes in FCGR2A [131R/R] LTRs. The gene discussed is CRP; the disease is endothelial dysfunction.