DLBCL-derived IL-8 interacted with its receptor (CXCR2) on neutrophils, resulting in the formation of NETs, which directly increased the expression of Toll-like receptor 9 (TLR9) pathways in DLBCL and subsequently activated the NFκB, STAT3 and p38 pathways, promoting tumor progression. This evidence concerns the gene STAT3 and diffuse large B-cell lymphoma.