In central nervous system (CNS) lymphoma, the balance between sOPN and iOPN activities has a pro-tumorigenic role, in which iOPN causes transcriptional downregulation of the NF-κB inhibitors, A20/TNFAIP3 and ABIN1/TNIP1, while sOPN promotes receptor-mediated activation of NF-κB [68]. Here, TNFAIP3 is linked to lymphoma.