Recent studies further showed that mutation of JAK2 was capable of inducing BCL [22, 23, 24], and inhibition of JAK2 decreased IgM-induced STAT3 phosphorylation and increased apoptosis of tumor cells in a dose-dependent manner, which suggest that JAK2 could be a target for the treatment of BCL [22, 25]. Here, JAK2 is linked to neoplasm.