How do Ras isoforms attain oncogenic specificity at the membrane? Oncogenic KRas, HRas, and NRas differentially populate distinct cancers. How they selectively activate effectors and why is KRas4B the most prevalent are highly significant questions. We also ask how Ras activates its effectors, including Raf and PI3K lipid kinase, which are also among the most highly mutated proteins in cancer. Despite decades of studies, major mechanistic questions are still unanswered. Broadly, we aim to figure out the hallmarks of oncogenic signaling in the cell.