But internal tandem duplications of the kinase domain (known as FLT3-ITD, found in about 20% of AML cases) and point mutations or deletions in the kinase domain (FLT3-TKD, present in about 10% of AML cases) have been shown to disrupt Ras signaling and upregulate expression of PDP1, a key regulator of the pyruvate dehydrogenase complex (41, 42). Here, FLT3 is linked to acute myeloid leukemia.