In addition, several microenvironmental targets such as IL-1β pathway and IL-1 antagonists or β3-AR agonists for sympathetic neuropathy (such as mirabegron) (260), mitochondrial heterocellular transfer, and inhibition by tigecycline, fatty acid oxidation (FAO) and FAO inhibitor etomoxir that sensitizes AML cells to therapeutic challenge, NO synthase inhibitors (such as cavtratin) (261, 262) and endothelium activation (59), are under investigation. This evidence concerns the gene IL1B and acute myeloid leukemia.