Mutant RAS activates several canonical growth factor signaling pathways, including the MAPK pathway (RAF/MEK/ERK) and the PI3K pathway (PI3K/AKT/mTOR). MAPK and PI3K signaling events take place in part on the surface of autophagic vesicles and lysosomes, respectively. Autophagy consists of the sequestration of damaged organelles within autophagic vesicles followed by fusion with the lysosome. A subset of known transcriptional regulators of autophagy genes are depicted, along with their regulation by growth factor kinase signaling pathways under the control of RAS. In this issue, Cheong et al. demonstrate that RAS-driven PI3K signaling increases levels of CK1α, which in turn phosphorylates and inhibits nuclear localization of FOXO3A, a transcription factor that positively regulates the expression of key autophagy genes (this pathway is denoted in yellow). Dashed lines indicate pathways described in other reports. Arrows indicate activation; lines ending in T indicate inhibition. UPR, unfolded protein response; TF, transcription factor.