Of note, Beltran et al. showed (25) that “concurrent loss of RB1 and p53 was present in 53.3% of NEPC patient tumors vs. 13.7% of CRPC-adenocarcinoma samples (P < 0.0004, proportion test).” In a classic NEPC genetically engineered mouse (GEM) model called TRAMP, p53 and RB1 are both inactivated in the prostate by SV40 large T antigen oncoprotein, which induces the development of prostate cancers that subsequently progress to NEPC (92). Here, TP53 is linked to adenocarcinoma.