Previous studies from our lab have shown that SULT1E1 expression either increases in the tumor with increased oxidative stress at late stages of the disease or reduces at the initial stages of the disease to let E2 be active and gradually increases with the disease pathogenicity [20], but remains inactive due to elevated oxidative stress, as shown in our animal studies (ENU paper) and another earlier studies. This evidence concerns the gene SULT1E1 and neoplasm.