Owing to the rapid kinetics of secondary tumour formation with GLSi, we reasoned that secondary tumours arose from pre-existing either late-stage pancreatic intraepithelial lesions or early PDAC (as opposed to in-transit metastasis) not detectable via ultrasound but likely present owing to the nature of the mice with pancreas-wide expression of oncogenic Kras and p53 heterozygosity. Here, KRAS is linked to neoplasm.