The Tor kinase is a key regulatory component that controls induction of autophagy. Tor-mediated control of autophagy may occur through at least 2 different mechanisms: direct phosphorylation of Apg13 and regulation of transcription by controlling the activation of phosphatases that regulate downstream transcriptional activators. As a general example, Tor phosphorylates the regulatory subunit Tap42 allowing it to bind and inhibit the PP2A-related Sit4 phosphatase. Inhibition of Tor allows the dissociation of Tap42 from Sit4; the activated Sit4 can now dephosphorylate and activate a regulatory protein that controls transcription of components that are required for autophagy. In autophagic induction, however, this process may be controlled by a regulatory subunit other than Tap42. Tor also causes the hyperphosphorylation of Apg13, which reduces its affinity for Apg1 and inhibits autophagy.