The pro-carcinogenetic effects of E2 are generally attributed to (a) E2/ER-mediated cell proliferation [17, 18]; (b) gene mutation initiated by catechol metabolites via cytochrome P450-mediated activation of E2 metabolism [17]; (c) aneuploidy through activation of aurora A [19] and (d) changes in chromosomal structures induced by E2 via ERR in both ER+ - and ER-- breast cancer cells [20]. This evidence concerns the gene ESR1 and breast carcinoma.