Therefore, although previous studies showed that HDAC inhibition can sensitize leukaemia cells towards 17‐AAG through HSP90 hyperacetylation resulting in increased 17‐AAG binding and increased client protein degradation (Rao et al., 2008; Scroggins et al., 2007), we postulate that acquired HSP90 inhibitor resistance is mediated by an epigenetic mechanism. Here, HDAC9 is linked to leukemia.