By analyzing the cytokine/chemokine profiles of the tumor cell-derived TME using mouse Lewis lung cancer and transgenic adenocarcinoma of the mouse prostate cell lines, we demonstrated that a population deficient in cluster differentiation 11b (CD11b) contributed to the anti-inflammatory environment in the TME, partly via secretion of a natural anti-inflammatory cytokine, IL1RN, and promoted tumor cell proliferation [29]. This evidence concerns the gene IL1RN and adenocarcinoma.