Since previous reports indicated that a putative p53 response element (RRRCWWGYYYN(0-13)RRRCWWGYYY) is located within human BTG2 promoter area and site-mutation of p53 response element abolished p53-dependent BTG2 induction in prostate cancer cells13, 14, 36, to further investigate the mechanisms whereby cisplatin modulates BTG2 expression in p53-wild LNCaP cells and p53-null PC-3 cells, we therefore applied 5′-deltion method and site-directed mutation of p53 response element, combined with BTG2 reporter assay, to further study. The gene discussed is TP53; the disease is Familial prostate cancer.