We recently demonstrated that mutant RAS, via its PI3K/AKT/mTOR effector signalling axis, upregulates the protein abundance of a ubiquitously expressed serine/threonine kinase, Casein Kinase 1 alpha (CK1α).29 We further showed that CK1α, but not CK1δ or CK1ε, phosphorylates and destabilizes nuclear FOXO3A to tightly regulate the level of basal autophagy in RAS-mutant cancer cells. Here, AKT1 is linked to cancer.