The proportion of precancerous or early lesions (AAH/AIS/Lepidic) (38.1%) in MET exon 14 skipping tumors was significantly higher than that of EGFR (15.9%), KRAS (5.6%), HER2 (21.9%), BRAF (15%), ALK (2.9%), RET (5.6%), and pan-negative (10.3%) lung adenocarcinomas, indicating that mutant MET alone might be insufficient to transform normal cells but depend on other genetic alterations progressing into more aggressive carcinoma subtypes. This evidence concerns the gene ALK and lung adenocarcinoma.