In addition, as mutant Kras is required for tumor formation in this model, we generated similar cohorts, but lacking mutant Kras (Pdx1-CreER Trp53R172H/+Atg7+/+, Atg7+/−, or Atg7−/−) to control for any phenotypes that were not associated with PDAC development (SI Appendix, Fig. S1A). The gene discussed is ATG7; the disease is neoplasm.