In CML-derived K562 cells, treatment with Imatinib increased the levels of phosphorylated p38, Chk2 and TA-p73, promoted co-localization between TA-p73 and PML, and induced TA-p73- and p38-dependent apoptosis [181]. The gene discussed is MAPK1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.