On this basis and our recent report demonstrating the role of metabolic reprogramming in conferring resistance to treatment with TKIs, we investigated the involvement of tumor-derived EVs (TDEs) in promoting drug-resistant phenotype in tumors and established a mechanism for this through upregulation of SLC1A5 in EVs of TKI-resistant cancer cell lines as well as in EVs from plasma of patients with TKI-resistant tumors. The gene discussed is SLC1A5; the disease is neoplasm.