In addition, although our in vitro study suggested that the TNF/IL1 low-expressing LCs are less responsive to JNK and NF-κB inhibitor treatment, we predict that our combined inhibitor treatment might also benefit these AML patients when combined with standard therapies because TNF and IL1 can be produced by bone marrow niche cells during chemotherapy or radiation therapy. This evidence concerns the gene IL1A and acute myeloid leukemia.