Epigenetic silencing of PTPN6, either due to DNA methylation or histone modification, as a contributive factor for deregulated JAK/STAT signaling has been previously described in various hematologic malignancies.[27, 28, 40] However, the role of PTPN6 mutations in DLBCL remains unclear. The gene discussed is SOAT1; the disease is hematologic disorder.