Besides genetic subtyping, AML can be characterized by shared signaling pathways and aberrant immunophenotypes such as co‐expression of CD7, CD56 (Chang et al, 2004), or a CD34lowGPR56high profile, the latter of which we associated with co‐mutations in NPM1, DNMT3A, and FLT3‐ITD (Garg et al, 2019), and high LSC frequency (Pabst et al, 2016). Here, FLT3 is linked to acute myeloid leukemia.