Recently researchers have found that the FLT3-C/EBPα-SCD axis affects fatty acid synthesis oxidation in AML patients with FLT3-ITD mutations, and that inhibition of FLT3 mutations leads to decreased expression of SCD1, resulting in an increase in PUFAs compared to MUFAs, and ultimately sensitization of AML cells to ferroptosis (Sabatier et al., 2023). This evidence concerns the gene FLT3 and acute myeloid leukemia.