By synthesizing multi-dimensional data from genomics, transcriptomics, proteomics, and metabolomics, researchers have successfully unveiled the molecular essence of tumor heterogeneity—from spatiotemporal evolutionary patterns of driver mutations (e.g., KRAS/TP53) to epigenetic dynamics of cancer stem cell subpopulations, and further to spatial topological features of metabolic-immune interactions at tumor invasion fronts. The gene discussed is KRAS; the disease is neoplasm.