So, heterozygous deletion of beclin1 has been associated with enhanced susceptibility to breast, ovarian, and prostate cancer in humans and increased spontaneous malignancies in mice [21]; Atg4C knockout mice have been shown to be more prone to develop chemically induced fibrosarcomas [22]; mosaic deletion of Atg5 in mice induced benign tumor development in the liver [23]; and tissue-specific Atg5 or Atg7 knockout increased the appearance of lung carcinomas driven by KRASG12D or BRAFV600E [24, 25], as well as KRASG12D-driven premalignant pancreatic lesions [26, 27]. Here, ATG5 is linked to benign neoplasm.