A large analysis of 29,757 FoundationCORE NSCLC samples found that ARID1A and EGFR were frequently comutated at diagnosis [37], indicating that ARID1A function is not critical for the survival of EGFR‐mutated NSCLC cells, and that ARID1A alterations may result in drug‐tolerant persister (DTP) phenotypes [48], which allow some NSCLC cells to survive EGFR TKI therapy, leading to clinical resistance. The gene discussed is ARID1A; the disease is non-small cell lung carcinoma.