Tumours from patients in cluster 5 had only few alterations in addition to the initiating KRAS mutations with increased MAPK pathway expression as well as high levels of PTEN. This implies that these patients’ tumours were driven by early PDAC events of hyperactive KRAS. In contrast, cluster 2 showed an enrichment of deletions in three major tumour suppressors (PTEN, RB1, and BRAC2). This evidence concerns the gene KRAS and neoplasm.