In a genetically engineered mouse model, sole Smarca4 knockout failed to induce lung adenocarcinoma, while concurrent introduction of p53 inactivation and Kras mutations resulted in robust development of highly penetrant undifferentiated carcinomas, indicating the requirement of additional genetic alterations in SMARCA4-deficit tumors to drive undifferentiated progression [26]. This evidence concerns the gene SMARCA4 and lung adenocarcinoma.