We also noted that it resembled what we have discovered previously in DLBCL samples associated with HBV infection7, with translocations in BCL6, copy number changes in NOTCH1 and CD70, and mutations in ZFP36L1, SGK1, IKZF3, TP63 and TP73. It has been shown that the HBV protein HBx can directly interact with CREBBP/EP300 and facilitate the recruitment of the complex onto CREB-responsive promoters, upregulating downstream oncogenes37. The gene discussed is SGK1; the disease is diffuse large B-cell lymphoma.