This latter property, albeit not clearly understood, may depend on the activation of key regulatory proteins in cancer cells, such as the tumour-suppressive p53 protein, which is activated by amifostine and can block cell proliferation in p53 WT tumour cells, or enhance apoptosis due to chemotherapeutic agents in p53 deficient-tumour cells [9-12]. The gene discussed is TP53; the disease is neoplasm.