Our results are consistent with other studies in which SFN treatment downregulates the expression of DNMT3B and HDAC1 [52, 53]. In vivo and in vitro studies have shown that SFN treatment for breast cancer, normal, hyperplastic, and cancerous prostate cells, human mesenchymal stem cells, nasopharyngeal carcinoma cells, colon cancer cells, and porcine satellite cells was found to significantly inhibit the activity of HDACs [9, 11, 46–48, 52–56]. The gene discussed is HDAC1; the disease is breast carcinoma.