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. The gene discussed is AKT1; the disease is prostate carcinoma.