Three cell lines with the CBFA2T3::GLIS2 fusion were responsive to ruxolitinib, CHZ868 and tofacitinib (type I inhibitor) in contrast to other AML models lacking the fusion, such as MOLM13 or MV4–11 (Fig. 4A and Supplemental Fig. 4A). This evidence concerns the gene GLIS2 and acute myeloid leukemia.