HDAC activity links the DNA damage and repair pathways.23 SFN could suppress HDAC activity and result in histone hyperacetylation in cancer cells.24 Among the class I HDACs, HDAC3 responded as the earliest one and was the most sensitive to SFN-suppressed protein expression.25 Therefore, we evaluated HDAC3 expression to verify its effect on the SFN-induced cell cycle arrest. The gene discussed is HDAC9; the disease is cancer.