Our study further demonstrated that exogenous CXCL10 activated the endogenous CXCL10/CXCR3 pathway through NF-κB in EGFR-mutant lung cancer cells, regardless of EGFR-TKI treatment; IFN-γ treatment and coculture with activated PBMCs increased endogenous CXCL10 in EGFR-mutant lung cancer cell lines, regardless of EGFR-TKI treatment; and CXCL10 siRNA treatment of EGFR-mutant lung cancer cell lines decreased CXCL10 in the supernatant. The gene discussed is CXCR3; the disease is lung cancer.