In particular, FLT3 methylation levels are maintained in AML cells even after TKI treatment, and limiting this activity with a pharmacological inhibitor improved FLT3-ITD+ AML cell elimination by a TKI, suggesting that PRMT1 inhibition might function as a therapeutic for AML patients with FLT3-ITD [45]. Here, PRMT1 is linked to acute myeloid leukemia.