Rosenfeldt et al. reported similar findings in Atg7-deficient KrasG12D/+ and Atg5-deficient KrasG12D/+ mice (driven by the Pdx promoter).33 Furthermore, the homozygous deletion of Trp53 in this model led to PDAC formation irrespective of autophagy, and shorter survival (due to tumour progression) in autophagy-deficient mice (both with Atg5−/− and Atg7−/− mice). The gene discussed is ATG7; the disease is neoplasm.