Therefore, it is likely that V9‐HFn‐Se metabolite selenocysteine inhibits HDACs and causes AML1‐ETO degradation, which leads to H3K9 acetylation, chromatin remodeling, change of gene expression profile, and differentiation and apoptosis of t(8;21) leukemia cells[21a,d] (Figure 6N). The gene discussed is RUNX1T1; the disease is leukemia.