For instance, AML1-ETO chimeric fusion protein, typical of AML patients with the translocation t(8;21)(q22;q22), recruits HDAC1, HDAC2, and HDAC3, silencing AML1 target genes, and therefore leading to differentiation arrest and transformation [53,54,55]. The gene discussed is RUNX1T1; the disease is acute myeloid leukemia.