Stabilizing IFNAR1 inhibits tumor growth and improves immunotherapy efficacy.26 The cytoplasmic domain of IFNAR1 is required for the phosphorylation of STAT1 at tyrosine-701 and subsequent STAT1 expression.21 IFNAR1 induces p-STAT1 and tumor immunity through modulating downstream immune checkpoint genes.27 Moreover, OX40L expression is dependent on p-STAT1 to reduce Th17 cell number and function in autoimmune diseases.28,29 Here, we showed that IFNAR1/p-STAT1 axis was involved in OX40/OX40L-mediated B-lymphoma cell interaction with Th17 cells in DLBCL. This evidence concerns the gene TNFRSF4 and diffuse large B-cell lymphoma.