Azacitidine, a therapeutic agent with DNA hypomethylating activity as the primary mechanism of action [53], inhibited ROS dependent NF-κB activation as well as STAT3 activation via restoration of SHP1, which is in line with a previous study using CD34 cells from AML patients [54] and anaplastic large cell lymphoma cells [55]. The gene discussed is STAT3; the disease is acute myeloid leukemia.