HDAC3, which is upregulated in prostate cancer (Weichert et al, 2008), facilitates lysine‐63‐chain polyubiquitination and phosphorylation of AKT in prostate cancer cells, a non‐nuclear effect mediated by AKT deacetylation at lysine 14 and 20 residues and HDAC3 interaction with the scaffold protein APPL1. This evidence concerns the gene AKT1 and Familial prostate cancer.