Interestingly, a recent study compared the genomic abnormalities observed in lung adenocarcinomas driven by mutant KRAS or EGFR and by overexpression of MYC; tumors from models driven by strong cancer drivers, such as mutant EGFR and KRAS, harbored few mutations in known cancer genes, whereas tumors driven by MYC acquired recurrent clonal KRAS mutations. This evidence concerns the gene EGFR and lung adenocarcinoma.