And although we did find alignment between growth effects in our model and human LUAD mutation rates in the context of EGFR—an oncogene notable for its low tumor mutational burden—most of the interactions we observed could not have been inferred from human data alone, e.g., with mutation rates overwhelmed by passengers for about 80% of the genes studied (Supplementary Fig. 11C, D) in the contexts of KRAS and BRAF. This evidence concerns the gene BRAF and neoplasm.