Specifically, to investigate whether disruption of RP-Mdm2-p53 signaling by Mdm2C305F mutation accelerates tumorigenesis induced by inactivation of pRb, we crossed Mdm2C305F mice with the well-characterized APT121 mouse prostate cancer model, in which a truncated SV40 large T antigen (consisting of the first 121 N-terminal amino acids; T121) controlled by the probasin promoter leads to pRb inactivation in prostate epithelium to induce prostate cancer [32], [33]. Here, MDM2 is linked to prostate cancer.