Given that an accumulation of LDs/SCD1 expression may be responsible for Gefitinib resistance and administrate with OA lead to induce LD expression and hyposensitivity to TKIs, we wondered whether combined targeting of EGFR and abnormal lipid metabolism can reverse resistance to Gefitinib in the indicated NSCLC cell lines. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.