Using this platform, the authors demonstrated that intratumoral DB1 activated TLR4 signaling in tumor-associated macrophages (TAMs), leading to IL-10 production and subsequent upregulation of IL-10 receptor (IL-10R) expression on multiple immune subsets, including CD8+ T cells, TAMs, and tumor-associated neutrophils (TANs) [299]. This evidence concerns the gene TLR4 and neoplasm.