In our study, we found that, in unresponsive tumours, where oncogenic EGFR signalling remained constitutively active, levels of immune cells in the TME were reduced compared to tumours that exhibited an active tumour response to therapy (Figure 1B–I), aligning with previous evidence that untreated EGFR-driven NSCLC mediates an immunosuppressive TME. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.