Other evidence supports the model of ATM-p53-Chk2, including: (a) Chk2 is not required for p53 responses in human cancer cells [27], (b) wild-type p53 suppresses mRNA and protein levels of Chk2 in human osteosarcoma Saos2 (p53 null) cells [28], (c) p53 mutations increase Chk2 expression in human gastric carcinoma [24], (d) Chk2 is dispensable for p53-mediated G1 arrest but is required for a latent p53-mediated apoptotic response [29], and (e) Chk2 expression is negatively regulated by functional p53, leading to a high level of expression in p53-deficient cancer cells [20, 30]. This evidence concerns the gene ATM and gastric carcinoma.