It may reflect the different effect of estrogen on cancer risk when it is taken orally, and our finding is supported by those of previous studies (59, 60) showing that oral intake of estrogen has its first-pass metabolic effect of suppressing hepatic production of insulin-like growth factor-I (IGF-I), a hormone partly interacting with CRP as a carcinogenic promotor, thus suggesting the protective role of exogenous estrogen in postmenopausal breast cancer risk (61). This evidence concerns the gene CRP and breast carcinoma.