CRP and cancer: Their low mutation frequencies (0.7–1.4%) argue that the promoter localization per se is not likely the cause of somatic hypermutation at the CRP-286 SNP -site in tumors; rather, the high incidence of the -286 mutation would be the result of functional consequences related to the enhanced induction of CRP, which may confer host cell clones sufficient advantage to survive and expand in the development of cancer.