As mentioned in Section 4.3.2, inhibition of NOX in FLT3-ITD AML cells suppresses STAT5 and oncogenic transcription to repress growth and survival, whereas mediators of oxidative stress such as nitric oxide and thiol redox reagents, through oxidation of crucial dithiols to disulphides within JAK2/3, inhibit interleukin 3-triggered in vivo activation, a phenomenon that is correlated with inhibited proliferation of lymphoid cells. This evidence concerns the gene FLT3 and acute myeloid leukemia.