AML is characterized by uncontrolled expansion and block in differentiation of leukemia stem cells (LSCs),[4] which are responsible for AML initiation, progression, and relapse.[5] LSC accumulation is caused by rearrangements, mutations, or aberrant expression of signaling nodes[6] that regulate LSC self‐renewal and differentiation.[7] Wnt/β‐catenin signaling is one of such signaling nodes, notably critical for LSC maintenance, with dishevelled 2 (DVL2) functioning as a principal Wnt component. The gene discussed is DVL2; the disease is acute myeloid leukemia.