Accumulating evidence suggests that the constitutive overexpresion of the inducible COX-2 gene is involved in a diverse array of cancers and Harris et al(20) demonstrated that COX-2 overexpresion initiated and promoted carcinogenesis through: i) mutagenesis, i.e., the production of certain reactive oxygen species that are carcinogenic; ii) mitogenesis, i.e., cell proliferation promoted by PGE-2 and other factors; iii) anti-apoptosis, i.e., cell differentiation and apoptosis reduced by PGE-2 and other factors; iv) angiogenesis, metastasis and immunosuppression (20). This evidence concerns the gene PTGS2 and cancer.