Autophagy controls cellular homeostasis by degrading long-lived proteins, protein aggregates, and defective organelles. It also suppresses tumorigenesis by limiting inflammation, eliminating toxic unfolded proteins, and removing damaged mitochondria that produce reactive oxygen species (which damage DNA). Loss of these protective events could promote cancer initiation (, ). Support for the tumor suppressive function of autophagy emerged from the findings that the gene encoding the essential autophagic protein Beclin 1 functions as a haplo-insufficient tumor suppressor in mice and humans (–). However, a comprehensive mechanistic view of how autophagy is turned off during tumor development and, more specifically, whether the tumor-suppressive activity of Beclin 1 results from its canonical autophagic function, was still missing. On page 956 in this issue, Wang et al. establish a connection between Beclin 1 and the Akt signaling pathway, which controls a large spectrum of cellular functions associated with cancer ranging from cell proliferation and survival to angiogenesis and metabolism. The finding underscores the importance of autophagy in tumor suppression