At the molecular level, the chromatin-modifying protein 1A was involved in the execution of the anacardic acid response and some activation of the ataxia telangiectasia mutated–p53 pathway was observed.31 Again, however, the role of the SUMOylation machinery was not investigated in this study, despite published evidence that anacardic acid reduces cellular overall SUMOylation.32 For example, in acute myeloid leukaemia (AML), anacardic acid reduced SUMO conjugation and increased cell death, especially in AML cells that were resistant to standard clinical chemotherapies.33 The gene discussed is TP53; the disease is acute myeloid leukemia.