In FLT3/ITD+ AML, a portion of mislocalized, underglycosylated RTK accumulates on the endoplasmic reticulum (ER) in a highly oxidized microenvironment where the RTK activates signal transducer and activator of transcription 5 (STAT5) through tyrosine phosphorylation, a phenomenon that does not occur with the mature fully glycosylated form, and there are high levels of localized reactive oxygen species (ROS) generated from ER-bound NADPH Oxidase 4 (NOX4)4, 6. Here, FLT3 is linked to acute myeloid leukemia.