However, these agentsfor the most part activate cell cycle arrest rather than death, andhigh doses in patients elicit on-target dose-limiting neutropenia.Recent work from our group indicates that combination of p53–MDM2inhibitors with the class-I HDAC inhibitor Entinostat (which itselfhas dose-limiting toxicity issues) has the potential to significantlyaugment cell death in p53 wild-type colorectal cancer cells. The gene discussed is HDAC9; the disease is Decreased total neutrophil count.