In leukaemia cells, chemotherapeutic drugs up‐regulate HDAC3 expression, and HDAC3 deacetylates AKT at K20, thereby promoting AKT phosphorylation, accelerating leukaemia progression and inducing chemotherapeutic resistance in MLL‐AF9(+) leukaemia cells.50 The gene discussed is AKT1; the disease is leukemia.