This interaction triggers activation of the catalytic domain and the subsequent dephosphorylation of the substrate.[5] Loss of function of PTPN6 in murine models has been previously described as a driver of autoimmune diseases.[6–8] Motheaten mice carrying the autosomal recessive motheaten (Ptpn6me) and viable motheaten (Ptpn6me-v) mutations were shown to develop immunodeficiency and several pathophysiological abnormalities.[7–9] In this study we investigated PTPN6 mutations in diffuse large B cell lymphoma and characterized their role in deregulation of STAT3 signaling pathway. This evidence concerns the gene PTPN6 and diffuse large B-cell lymphoma.