In this respect, despite a potential limitation being the evaluation of A17pro anti‐cancer activity in only the one mutant KRAS PDX model, our current findings nonetheless pave the way for future studies to validate the driver role of ADAM17 in additional mutant KRAS LAC PDX models, as well as other PDX models for different lung cancer subtypes (e.g., wild‐type KRAS LAC, mutant EGFR LAC, and squamous cell carcinoma). This evidence concerns the gene LCT and lung carcinoma.