Autophagy is a highly conserved catabolic process in which cells degrade and recycle their own constituents through lysosomal degradation machinery.The physiological function of autophagy is essential for cell survival, differentiation, development, and homeostasis.Atg9 has been shown to be the only transmembrane Atg protein and is thought to act as a potential membrane carrier for forming autophagosomes.However, the physiological function of Atg9 remains elusive.Our recent study has shown that Drosophila Atg9 regulates the c-Jun N-terminal kinase (JNK) activity through interacting with Drosophila tumor necrosis factor receptor-associated factor 2 (dTRAF2) under oxidative stress conditions.ROS-induced autophagy dissociates Atg9-dTRAF2 interaction, leading to diminish JNK activation, thereby helping the maintenance of tissue homeostasis.We further found that Atg9 knockdown resulted in shortened lifespan and decreased stress tolerance in adult fly.Similar phenotypes were observed in Atg9 mutant animals.The molecular regulation of Atg9 in these processes will be discussed.