Additionally, SFN also indirectly upregulated NRF2 expression by enhancing binding between NFE2L2 promoter and active chromatin marker acetylated histone 3 (Ac-H3), while the protein level of Ac-H3 could be increased by prominently attenuated HDAC1, 4, 5, and 7 or impaired formation of the transcriptional regulator complex partly consisted of DNMT and HDAC after SFN treatment in prostate cancer (Zhang et al., 2013) and breast cancer (Sharma et al., 2005; Saxena and Sharma, 2010; Meeran et al., 2012) respectively, restoring the cellular antioxidant and detoxification effects. The gene discussed is HDAC9; the disease is prostate cancer.