To investigate the effect of drugs targeting the mechanisms responsible for the aberrant stabilization of mutant p53 in cancer cells, specifically HSP90 and its indispensable regulator HDAC6 [11, 12, 54], we examined two HSP90 inhibitors, 17-N-allylamino-17-demethoxygeldanamycin (AAG) and Ganetespib (Ganet), as well as the potent HDAC inhibitor Suberoylanilide hydroxamic acid (SAHA). The gene discussed is HDAC9; the disease is cancer.