Although the conditional LSL-KrasG12D/+;LSL-Trp53R172H/+;Pdx1-Cre (KPC) model (Hingorani et al., 2005) of PDAC demonstrated a close mimicking of the human disease, it lacked inducible control of Kras. This type of control over mutant Kras expression allowed for the study of its role in primary and metastatic tumor maintenance when expressed concurrently with mutant p53 (Collins et al., 2012b) and the demonstration of mutant Kras-dependence on more aggressive and metastatic pancreatic cancer. The gene discussed is KRAS; the disease is metastatic neoplasm.