Several molecular alterations are known to be involved in tumorigenesis of lung adenocarcinoma, such as epidermal growth factor receptor (EGFR), Kirsten rat sarcoma viral oncogene homolog (KRAS), v-raf murine sarcoma viral oncogene homolog B (BRAF), human epidermal growth factor receptor 2 (HER2), and echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) fusion mutations. This evidence concerns the gene BRAF and lung adenocarcinoma.