Thus, the intratumoral GC activated DCs in three possible ways: (1) GC, mainly taken up by neutrophils (Figure 2C), mediated the glycosylation-dependent interactions between neutrophils and DCs to activate DCs and promote the migration of mature DCs into TDLNs; (2) GC increased the secretion of TNF-α in serum, which then contributed to the neutrophil mediated maturation of DCs 45, 47; (3) DCs ingested some GCs (Figure 2C and Figure S3B) and, in combination with LIT-induced immunogenic tumor cell death and the release of DAMPs (Figure 2G), promoted the maturation of DCs. The gene discussed is TNF; the disease is neoplasm.