In the buffy mutant, increased target of rapamycin (Tor) signaling and altered basal energetics, hypothesized to be due to reduced metabolic efficiency, are both required for the precocious autophagy phenotype and collaborate in the inability to survive nutrient stress. Increased Tor signaling in fed animals fuels energy-intensive, growth-promoting processes. This is balanced by the altered energy metabolism as demonstrated by reduced lipid and glycogen storage and lack of overgrowth phenotypes. It is possible that the increase in Tor signaling is due to altered metabolism or that the two are independent of each other. However, the altered metabolism cannot entirely be due to increased Tor signaling because ectopic expression of activated S6K does not recapitulate precocious autophagy in a wild-type background. Upon starvation, loss of Tor signaling releases inhibition of autophagy while phosphorylated S6K promotes autophagy. Our data demonstrates that a second Tor-independent, nutrient-responsive input is required for precocious autophagy. This second input is hypothesized to arise from the altered basal energetics uniquely found in buffy mutants.