Our study demonstrates that CXCL10, a representative inflamed immune-response cytokine, activates CXCR3 in tumor cells to induce the phosphorylation of Src and the NF-κB subunit, p65, and the expression of HIF1-α in persistent EGFR-mutant tumor cells during EGFR-TKI treatment. The gene discussed is HIF1A; the disease is neoplasm.