Finally, concomitant with cell cycle arrest, theunderlying molecular mechanisms of Mtx-C in AML cells include myeloiddifferentiation, as evidenced by the increased expression of PU.1,myeloperoxidase, CD15, CD11b, and CD14 in the AML and LSC populationswith the participation of p38 mitogen-activated protein kinase. The gene discussed is FUT4; the disease is acute myeloid leukemia.