A minority of these studies is based on mutant p53 KI mouse models and led to a number of discoveries in the field, including (i) the inhibitory role of mutant p53 on MRE11 protein and the induction of genomic instability (human TP53 KI “HupKI” mouse model) (21), (ii) the transcription-based activation of PDGFRβ signaling in pancreatic cancer model (22), (ii) the transcriptional activation of oncogenic Pla2g16 phospholipase (23), and (iv) the confirmation of prior cell-based reports on a mutant p53-mediated inhibition of the p63/p73 oncosuppressive activity (12, 18). The gene discussed is TP53; the disease is pancreatic neoplasm.