Interestingly, although mutations in FLT3 may be driver mutations in AML, it is known that they cannot induce disease development on their own and require other helper mutations during leukemogenesis, including chromosomal alterations such as t(8; 21) (q22; q22); RUNX1‐RUNX1T1, inv(16) (p13.1q22); CBFB‐MYH11 and t(15; 17) (q22; q12); PML‐RARA, as well as point mutations in genes such as NPM1 and DNMT3A with which frequent coexistence has been found in patients with AML with normal karyotypes.14 Here, DNMT3A is linked to acute myeloid leukemia.