Despite both being driven by mutant Kras and loss of normal Trp53 function, differences in the autochthonous KP-/-C and KPC PDAC models are known and have been attributed to differences in tumor latency and p53 status, as well as differences in how stromal cell populations interact with cancer cells to support tumor growth (Rosenfeldt et al., 2013; Vennin et al., 2019). Here, KRAS is linked to neoplasm.