In the context of cancer, the role of autophagy is controversial and resembles the mythical ‘janus face’. Autophagy plays tumor suppressive function by clearing unfolded proteins or damaged organelles, thereby preventing genome instability.6, 7, 8 Loss of autophagy genes perturbs homeostasis and potentially primes cells for tumor development. Many core autophagy genes, including BECN1, UVRAG, SH3GLB1 (Bif-1), ATG2B, ATG5, ATG9B, ATG12 and RAB7A, are frequently mutated in human cancers.9 In various murine models, depletion of essential autophagy genes promotes tumorigenesis. Heterozygous disruption of BECN1 leads to spontaneous tumor formation in mice, indicating BECN1 is a halpoinsufficient tumor suppressor,10, 11, 12 mice lacking ATG5, ATG7 or AMBRA1 show similar effect.13, 14, 15 However, autophagy is also involved in oncogenic process in some circumstances. Autophagy promotes tumor cell survival and growth within tumor microenvironment, such as hypoxia or metabolic stress. Dysfunction in autophagy pathway suppresses tumor proliferation, dissemination and metastasis.15 Inhibition of autophagy increases sensitivity of tumor cells to chemotherapeutic agents as well as radiation therapy.16, 17, 18 Deletion of FIP200, a component of the ULK1–ATG13–FIP200 complex that is required for autophagosome formation, suppresses tumor initiation and progression. These findings strongly support the role of autophagy in oncogenesis in vivo.19