According to the potential mechanisms related to ARID1A, we summarized that the small molecular inhibitors targeting ARID1A or PI3K/Akt signaling pathway, the anti-angiogenic therapy and immunotherapy could be used as the supplementary treatment for EGFR-TKIs among NSCLC patients harboring the concomitant alterations of sensitive EGFR mutations and ARID1A. The mechanisms related to ARID1A alterations and expression loss in inducing the resistance to EGFR-TKIs are displayed in Fig. 1. This evidence concerns the gene ARID1A and non-small cell lung carcinoma.