Also, vorinostat showed apoptotic and antiproliferative effects on CRC cell lines in vitro in combination with another pan-HDAC inhibitor, trichostatin A. This treatment induced the attenuation of Wnt signaling due to proteasome-dependent degradation of the Wnt transcription factor TCF7L that was HDAC6 dependent [165]. The gene discussed is HDAC9; the disease is colorectal carcinoma.