Several potential causes have been suggested and studied including deregulated cytokine secretion (e.g. IL-10), [21] gain of function mutations, [22–24] and loss of negative regulators of JAK/STAT signaling such as SOCS1 [25–27] and protein tyrosine phosphatases.[28, 29] Protein tyrosine phosphatases (PTP) are important enzymes that negatively regulate the activity of multiple signaling pathways downstream of tyrosine kinases including the Janus kinases.[1, 30, 31] However, the role of PTPN6 mutations in the regulation of STAT signaling has not previously been described in DLBCL. This evidence concerns the gene SOAT1 and diffuse large B-cell lymphoma.