It is known, in fact, that the BCR/ABL fusion protein in CML cells, promotes the accumulation of p53 and that, in contrast to the activation of p53 by c-Abl, its oncogenic form, BCR/ABL, counteracts the growth inhibitory activities of p53 by modulating the p53-MDMD2 loop. The gene discussed is TP53; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.