AR and neoplasm: Contrary to HATs resulting in the increased acetylation of histones or AR, the activity of deacetylases such as SIRT1 or SIRT2 can regulate cellular growth and sensitivity to ADT therapy through AR deacetylation [121], and the use of small molecule inhibitors has been shown to effectively reduce tumour growth, EMT and metastasis, and sensitize mCRPC to ADT therapy (Figure 1) (Table 1) [23,27,122].