In the present study, we have demonstrated that inhibition of BCR/ABL, Jak2-V617F, and FLT3-ITD, which represent the most frequently found aberrantly activated tyrosine kinases in CML, BCR/ABL-negative myeloproliferative neoplasms, and AML, respectively, downregulated Chk1 activation as well as G2/M cell cycle arrest and drastically enhanced apoptosis induced by chemotherapeutic agents, etoposide and doxorubicin (Fig. 1–4). The gene discussed is ABL1; the disease is myeloproliferative neoplasm.