We observed therapeutic intervention including midostaurin decimated most AML clones including the dominant AML clone at presentation (i.e., C2, WT1+/NPM1+/FLT3‐TKD+) but provided potent selective pressure for the survival and expansion of a relapse‐fated subset of C3, C3‐ITDHom. The gene discussed is WT1; the disease is acute myeloid leukemia.