HDAC9 and cancer: Z16 induced SMC3 hyperacetylation at low concentrationsand histone hyperacetylation at high concentrations, which can beexplained by HDAC8 degradation and off-target HDAC inhibition, respectively.Importantly, Z16 potently inhibited proliferation ofvarious cancer cells at low micromolar concentrations via differentantiproliferative mechanisms, which can, to a large extent, be attributedto off-target HDAC inhibition instead of HDAC8 degradation.