It was shown that CD11b(+)Gr-1(+) myeloid cells can protect proliferating tumor cells from senescence or enable already arrested cells to escape from oncogene-induced senescence by antagonizing senescence in a paracrine manner through interfering with the SASP of the tumor and secretion of interleukin-1 receptor antagonist (IL-1RA) [19]. Here, ITGAM is linked to neoplasm.