While it was important to see that the effects of loss of Atg7 on primary tumor development in this model were similar to our studies on PDAC in mice driven by mutant Kras and deletion of Trp53 (10), it was striking and unexpected to see that hemizygous loss of Atg7 also had an effect on the number of animals with PanINs and PDAC when compared with animals wild-type for Atg7. The gene discussed is KRAS; the disease is neoplasm.