KRAS is mutated in >90% of PDACs, but even most tumours with wild-type KRAS contain somatic genetic alterations that activate the RAS/mitogen-activated protein kinase pathway upstream or downstream of KRAS, suggesting that the RAS pathway remains an important molecular driver of pancreatic tumorigenesis even in the absence of KRAS mutations.7 Inactivating mutations in TP53 are the second most common genetic alteration occurring in ~70% of PDACs.8,9. Here, TP53 is linked to neoplasm.