Observational mechanistic study in relapsed/refractory DLBCL treated with selinexor + lenalidomide + rituximab. Selinexor: oral selective inhibitor of nuclear export (SINE) that blocks XPO1, retaining tumor suppressors (e.g., p53) in the nucleus, suppressing NF-kB/oncogenic transcription and inducing apoptosis in lymphoma cells. Lenalidomide: oral immunomodulatory drug (IMiD) that binds cereblon, causing IKZF1/3 degradation, boosting T- and NK-cell activation, cytokines, and anti-tumor immunity, enhances ADCC. Rituximab: anti-CD20 monoclonal antibody targeting malignant B cells, mediating ADCC, CDC, and apoptosis. Targets/pathways: CD20+ B cells, XPO1-mediated nuclear export, tumor suppressor and NF-kB pathways, cereblon-IKZF axis, NK/T effector function and ADCC. The study profiles blood/tumor immune subsets to link mechanisms with response/resistance.