In conclusion, we showed for the first time that: (a) S100P binds p53 protein and increases its level, (b) this binding leads to reduced p53 phosphorylation and transactivation activity in response to DNA damaging treatments, (c) through the inactivation of p53, S100P permits the onset of therapy-induced senescence and supports survival of the drug-treated tumor cells (see the scheme on Figure 7D). This evidence concerns the gene S100P and neoplasm.