One study suggested that both p53R172H and p53-null cells escape KRASG12-induced growth arrest/senescence in pancreatic cancer; nevertheless, only mice expressing mutant p53R172H developed pancreatic ductal adenocarcinoma (PDAC), which indicated a novel role played by mutant p53 that is different from that of p53 knockout [16]. This evidence concerns the gene TP53 and familial pancreatic carcinoma.