This strategy has added clinical relevance, since, in ESCC, EGFR expression is inversely correlated with immune-cell infiltration, indicating that EGFR-driven ESCC is unlikely to respond well, or durably, to immune checkpoint inhibitor therapy (CPI) [18] as shown by the limited efficacy of CPIs in mutant-EGFR-driven NSCLC [19, 20]. The gene discussed is EGFR; the disease is esophageal squamous cell carcinoma.