A first model of chronic liver damage has initially demonstrated that proliferating stellate cells deficient for p53 were able to stimulate polarization of macrophages into a tumor-promoting M2-state and enhance the proliferation of premalignant cells (99) Since then, many studies focused on the clinical and prognostic implication of p53 on macrophage infiltration in some cancers and revealed that patients with mutant TP53 had significantly higher macrophage infiltration than those with wild-type TP53 and this was correlated with poorer survival (100). This evidence concerns the gene TP53 and cancer.