In addition, SFN (at 15 μM) was also found to be an efficient HDAC inhibitor in BPH-1 (benign prostatic hyperplasia), LnCaP (lymph node carcinoma of the prostate) and PC-3 (prostate epithelial) cells by triggering growth arrest and apoptotic processes [183]. This evidence concerns the gene SFN and benign prostatic hyperplasia.