AKT1 and prostate cancer: By treating AR‐positive prostate cancer C4‐2 cells with the commonly used pan class I/II HDACIs trichostatin A (TSA), suberoylanilide hydroxamic acid (SAHA), panobinostat (LBH589), and HDAC6‐selective inhibitor tubastatin A, we demonstrated that these pan class I/II HDACIs, but not tubastatin A completely inhibited AKT phosphorylation at S473 and T308 (Fig 1A).