Given the major importance of the oncogenic fusion protein BCR-ABL (carries aberrant tyrosine kinase activity) in t(9;22) CML (chronic myeloid leukemia) patients, a pivotal role of aberrant HDAC2 function in CML pathogenesis is herein suggested to occur. The gene discussed is HDAC2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.