GSTP1 and infection: These results support the hypothesis of De Marzo and his colleagues, and suggest that loss of GSTP1 gene expression, probably as a result of hypermethylation of the CpG island sequences of GSTP1, will render the prostatic epithelial cells more vulnerable to genomic damage mediated by the infection itself or by the oxidant carcinogens elaborated by inflammatory cells (neutrophils, lymphocytes, and macrophages) (Nelson et al, 2003).