A non-cell autonomous mechanism of tumor suppression by p53 has been described through skewing of macrophage polarization toward the tumor-inhibiting M1-subtype; selective p53 deletion in the myeloid lineage led to elevated levels of inflammatory cytokines and a significant increase in tumor initiation whereas mild activation of p53 in the myeloid lineage restricted tumor progression (199, 200). Here, TP53 is linked to neoplasm.