Selected candidate molecules were further validated in genetically engineered mouse models of PDAC with mutated Kras (KC mice) or with mutated Kras and TP53 (KPC mice) and associated with PDAC initiation and progression (PanIN‐PDAC) (Hingorani et al, 2003, 2005; Capello et al, 2013), as well as in patient‐derived PDAC xenografts (PDAC‐PDX), where their levels correlated with tumor burden and response to treatment. Here, KRAS is linked to neoplasm.