SAHA arrests cancer cell growth by inhibiting classes I and II zinc‐binding HDACs.5, 6 Substantial evidence indicated that SAHA induced histone acetylation in transcription factor complexes that regulate the genetic expression of molecules associated with malignant phenotypes.7 Similar to HDACi, ING5 may form MOZ/MORF‐BRPF1/2/3‐ING5‐hEaf6 and JADE1/2/3‐HBO1‐ING4/5‐hEaf6 HAT complexes to acetylate histones H3 and H4, respectively.8 The gene discussed is MEAF6; the disease is cancer.