Nevertheless, it still displays limited clinical efficacy in some NSCLC patients, which results from EGFR‐dependent (e.g., C797S mutation or some rare mutations) or EGFR‐independent (e.g., RAS/BRAF‐V600E mutations, MET/HER2 amplifications, RAS‐MAPK/PI3K‐AKT pathways activation, or oncogenic fusion) mechanism of drug‐resistant [54]. This evidence concerns the gene BRAF and non-small cell lung carcinoma.