Transcription factor FOXM1 and Six1/TCF7L2 upregulation activate Wnt–β-catenin signaling pathways by directly binding to β-catenin and stabilizing the β-catenin protein, thereby preserving LSC quiescence and promoting LSC self-renewal in MLL-rearranged AML [62,63]. The gene discussed is KMT2A; the disease is acute myeloid leukemia.