The study by Noda and Ohsumi investigates the role of Tor, a phosphatidylinositol kinase homologue, in controlling autophagy in yeast. They found that Tor negatively regulates autophagy induction, as rapamycin, an inhibitor of Tor function, induces autophagy even in nutrient-rich conditions. Temperature-sensitive tor mutants also exhibit autophagy induction at nonpermissive temperatures. The authors further show that high concentrations of cAMP inhibit autophagy induction. Autophagy is not induced in *apg* mutants, suggesting that the site of action of Tor is upstream of Apg proteins. In nutrient-rich media, Apg proteins are involved in the transport of aminopeptidase I to the vacuole. Tor may act to switch Apg function between autophagy and the transport of aminopeptidase I. The study highlights the involvement of Tor in the starvation-signaling pathway of autophagy and provides insights into the regulatory mechanisms of autophagy in yeast.The study by Noda and Ohsumi investigates the role of Tor, a phosphatidylinositol kinase homologue, in controlling autophagy in yeast. They found that Tor negatively regulates autophagy induction, as rapamycin, an inhibitor of Tor function, induces autophagy even in nutrient-rich conditions. Temperature-sensitive tor mutants also exhibit autophagy induction at nonpermissive temperatures. The authors further show that high concentrations of cAMP inhibit autophagy induction. Autophagy is not induced in *apg* mutants, suggesting that the site of action of Tor is upstream of Apg proteins. In nutrient-rich media, Apg proteins are involved in the transport of aminopeptidase I to the vacuole. Tor may act to switch Apg function between autophagy and the transport of aminopeptidase I. The study highlights the involvement of Tor in the starvation-signaling pathway of autophagy and provides insights into the regulatory mechanisms of autophagy in yeast.