For instance, combination studies in vitro suggest that the biological crosstalks between the c-MYC, PI3K/AKT/mTORC1, STAT3, IRF4 and/or BCR/NF-κB-dependent signaling pathways represent promising targets in a subset of ABC-DLBCL that may be exploited for a combination therapy of relapsed/refractory DLBCL together with cytotoxic (immuno-)chemotherapeutic agents, that are currently used to treat ABC-DLBCL [313, 595, 596]. Here, NFKB1 is linked to diffuse large B-cell lymphoma.