HDACi treatment induced the inhibition of lung cancer cell growth, cell growth arrest at G2/M phase, and apoptosis evidenced by caspase 3 cleavage at comparable IC50 concentrations to that of SAHA (also known as Vorinostat), the only HDACi currently approved for the clinical treatment of cutaneous T-cell lymphoma [23–25]. This evidence concerns the gene CASP3 and lung carcinoma.