Given that both AKT and AR signaling are aberrantly activated in prostate cancers, especially those with PTEN deletions or SPOP mutations, dual inhibition of AKT and AR pathways by administrating the single‐agent HDAC3 inhibitor makes HDAC3 inhibition an attractive strategy for prostate cancer treatment in the clinic. The gene discussed is AKT1; the disease is prostate carcinoma.