NF-κB is a well-recognized target of MCL whose activity is greatly inhibited by MCL.14–16 In addition, MCL was reported to elevate intracellular reactive oxygen species to induce apoptosis of malignant cells.18,44 NF-κB, which is systemically activated in MPNs, is a key transcriptional factor that promotes inflammatory responses and is required for maintenance of tumor stem cells.41,45 Accordingly, NF-κB may be correlated with the observed reduction of cytokines and JAK2V617F mutant allele burden caused by MCL in Jak2 mice. This evidence concerns the gene JAK2 and neoplasm.