A recent study evidenced that conditional homozygous deletion of histone deacetylase (HDAC) 3, AKT inhibition, and AR reduction in PTEN-deficient mouse models suppresses prostate tumorigenesis and progression [73], suggesting in the HDAC 3 inhibition together with PTEN inducers new possible therapeutic approaches for prostate cancer patients. The gene discussed is AKT1; the disease is prostate carcinoma.