It is reported that AF could bind to the SeC-containing C-terminal and the N-terminal redox center to inhibit TrxR activity [37], and PL probably directly binds to and inhibits the antioxidant enzyme glutathione S-transferase pi 1 (GSTP1) and carbonyl reductase 1 (CBR1), resulting in elevated levels of ROS and subsequent cancer-selective cell death [16, 17]. This evidence concerns the gene CBR1 and cancer.