Notably, SETD2 mutations often cooccur with other well-established driver mutations, such as KRAS, EGFR, and BRAF, that activate the RTK/RAS/RAF pathway in lung adenocarcinoma (12), suggesting that SETD2 inactivation probably cooperates with these driver mutations to promote lung tumorigenesis. Here, SETD2 is linked to lung adenocarcinoma.