We speculate that mutation in B-Raf proto-oncogene may contribute, at least in part, to NRF2-mediated NQO1 overexpression to drive HCC development and that SFN treatment enhances oncogenic B-Raf-associated NRF2 activation, thereby up-regulating NQO1 expression to stimulate tumor growth. Here, BRAF is linked to hepatocellular carcinoma.