We have previously shown that mutant RAS, via its PI3K/AKT/mTOR effector signalling axis, upregulates the protein abundance of CK1α, leading to phosphorylation-driven destabilization of nuclear FOXO3A in RAS-mutant cancer cells.29 In the present study, we further showed that CK1α proteins are upregulated in both cytoplasm and nuclei of RAS-mutant cancer cells (Supplementary Figure 7a). The gene discussed is FOXO3; the disease is cancer.