KMT2A and acute myeloid leukemia: Therefore, understanding β-catenin function in MLL-LSCs highlighted this pathway as a possible therapeutic target for the selective elimination of AML-LSCs.130, 131, 132 Suppression of COX as an abrogator of β-catenin in fully developed MLL-AF9-induced leukemia decreased both β-catenin and the frequency of LSCs.