In addition, Th17 cells can modulate immune cells, endothelial cells and stromal cells, inducing an immunosuppressive tumor microenvironment.24 In DLBCL, Th17 cells were reported to provoke rituximab resistance by suppressing p53 expression and inhibiting cell apoptosis.25 To our knowledge, this study provides direct evidence that serum miR130b contributed to DLBCL progression through Th17-asscociated immunosuppressive microenvironment. This evidence concerns the gene TP53 and neoplasm.