SOX4 expression is thought to support self-renewal of leukemic cells and to inhibit differentiation in C/EBP α-mutant AML [55], support PI3K/Akt signaling in BCR-ABL-driven B-ALL [53], and cooperate with Pu.1 haploinsufficiency in murine leukemia [54]. This evidence concerns the gene SPI1 and acute myeloid leukemia.