These results agree with a recent study of Atg7 deletion in pancreatic cancer to suggest deficient autophagy may augment tumor activity and metabolism.40 In that study and others, it appears that apoptotic impairment, for example, via p53 deletion, may be vital to turn pro-proliferative effects of Atg gene deletion into malignant benefits.40,41 As apoptosis is affected by MLL–ENL,35,42 our results support this hypothesis. This evidence concerns the gene TP53 and familial pancreatic carcinoma.