Next, since we observed that doxorubicin treatment induced a clear increase in miR-125b expression in NPM-ALK(+) ALCL cells (Figure 6A), and since its major target is DNA topoisomerase II (Topo II), a DNA-binding protein required for the maintenance of DNA methylation by DNMT1 [22, 23], we assessed the role of Topo II in miR-125b regulation by treating cells with etoposide, a Topo II inhibitor that is part of the CHOEP (cyclophosphamide, doxorubicin, vincristine, etoposide and prednisone) chemotherapy regimen, at final concentrations ranging from 100 to 300 nM. Here, ALK is linked to anaplastic large cell lymphoma.