In Burkitt lymphoma (BL), BCL6 deficiency induced JAK2 expression and STAT3 phosphorylation, and a JAK2 inhibitor, Lestaurtinib, repressed survival of BCL6-deficient cells and tumor xenografts, demonstrating the significance of co-suppressing BCL6 and JAK2, which was considered as synthetic lethality [58]. This evidence concerns the gene JAK2 and neoplasm.