Previous studies have revealed that hyperacetylation of HSP90 induced by HDAC6 depletion or HDAC inhibitors would restrain the chaperone function of HSP90, thereby promoting the polyubiquitylation and proteasomal degradation of client proteins, like c-Raf, Akt, cyclin D1, and ERα, to evoke growth arrest and apoptosis of cancer cells (9, 51). The gene discussed is HDAC9; the disease is cancer.