The studies carried out in FLT3-ITD+ AML cells have shown that the DEP-1 protein is expressed in these cells, but was unable to function as an inhibitor of FLT3-ITD signaling; this is due to the high ROS levels in FLT3-ITD+ cells leading to partial inactivation of DEP-1 by reversible oxidation [42]. The gene discussed is PTPRJ; the disease is acute myeloid leukemia.