1. Tsai, F. D. et al. K-Ras4A splice variant is widely expressed in cancer and uses a hybrid membrane-targeting motif.Proc. Natl Acad. Sci. USA112, 779–784 (2015).2. Voice, J. K., Klemke, R. L., Le, A. & Jackson, J. H. Four human Ras homologs differ in their abilities to activate Raf-1, induce transformation, and stimulate cell motility. J. Biol. Chem.274, 17164–17170 (1999).3. Kimmelman, A. C. Metabolic dependencies in RAS-driven cancers.Clin. Cancer Res.21, 1828–1834 (2015).4. Ying, H. et al. Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism.Cell149, 656–670 (2012).5. Kerr, E. M., Gaude, E., Turrell, F. K., Frezza, C. & Martins, C. P. Mutant Kras copy number defines metabolic reprogramming and therapeutic susceptibilities.Nature531, 110–113 (2016).