FLT3 and acute myeloid leukemia: Therefore, to better understand the role and regulatory mechanism of Gln metabolism in oxidative homeostasis of AML, one study using a FLT3-mutated AML cell model found that impaired Gln metabolism by FLT3 inhibitors could lead to depletion of GSH and accumulation of mitochondrial reactive oxygen species (mitoROS), subsequently leading to apoptosis of AML cell (48).