According to a study, approximately 20% of NSCLC patients who developed resistance to first-generation EGFR TKIs erlotinib or gefitinib showed upregulated AXL expression, and about 25% showed upregulated GAS6 expression (45) In preclinical models, AXL has been shown to mediate resistance of NSCLC cells to first-, second-, and even third-generation EGFR TKIs through activation of bypass signaling pathways such as PI3K/AKT, MAPK/ERK, and NF-κB. This evidence concerns the gene NFKB1 and non-small cell lung carcinoma.