TGFBR2 deficiency in an APC-deleted mouse model of intestinal adenoma increased inflammatory burden and promoted tumor progression via producing tumor necrosis factor-α (TNF-α), interleukin (IL)-8, and TGF-β1 as well as suppressing of anti-inflammatory cytokines such as IL-10 and interferon (IFN)-γ, which resulted in increased infiltration of CD11b+Gr1+ granulocyte population into the tumor microenvironment (Figure 2) [45]. This evidence concerns the gene CXCL8 and neoplasm.