Besides a novel JAK/STAT-PIM2/3 axis-mediated compensation pathway discovered in this study, accumulating evidence (our previous studies and others) also suggests that non-canonical NFKB2 pro-leukemia inflammatory pathways could play an essential role in treatment-resistance in both standard treatments and targeted therapies for AML (60, 71). This evidence concerns the gene SOAT1 and acute myeloid leukemia.