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). The gene discussed is PIM2; the disease is acute myeloid leukemia.