Following the demonstration that HDAC inhibitors enhanced radiation-induced clonogenic suppression of experimental in vitro and in vivo colorectal carcinoma models [6]–[9], but independently of the actual histone acetylation level at the time of radiation exposure [7], [8], we conducted the Pelvic Radiation and Vorinostat (PRAVO) phase 1 study [10], [11]. Here, HDAC9 is linked to colorectal carcinoma.