NSCLC patients with EGFR mutations with low APEX1 expression achieved longer PFS and OS time after treatment with EGFR-TKI, and APEX1 protein levels were significantly elevated in EGFR-TKI-resistant cell lines, APEX1 activates Akt signaling in lung adenocarcinoma through a redox-dependent mechanism, which stimulates epidermal growth factor receptor-TKI resistance, a specific APEX1 inhibitor (APX3330) can make cells more sensitive to EGFR-TKI (Lu et al., 2018; Yang et al., 2018). Here, APEX1 is linked to lung adenocarcinoma.