Since we detected p53-dependent up-regulation of Mdm-2 expression (Table 1) in HCT116p53+/+ cells, and Mdm-2 was shown to bind FAK to down-regulate p53, providing survival to cancer cells [11], we used compound M13 that disrupted interaction of FAK and Mdm-2, called M13 that up-regulated p53 activity and caused apoptosis in HCT116 p53+/+ cells [14] in combination with R2 in clonogenicity assay to test if combination of R2 and M13 will decrease cancer cell clonogenicity more effectively than each agent alone. This evidence concerns the gene MDM2 and cancer.