Furthermore, two xenografts were employed to confirm a hyposensitization to Gefitinib by OA and the reversal of Gefitinib resistance by the combination of g-PPT and Gefitinib Altogether, these results demonstrate that abnormal LD accumulation, SCD1 and lipid metabolism are candidate therapeutic targets for the treatment of TKI-resistant EGFR-mutant NSCLC and highlight the importance of detecting lipid metabolism in tumors to predict the emergence of EGFR-TKI resistance. This evidence concerns the gene EGFR and non-small cell lung carcinoma.