Numerous studies in human NSCLC patients or a mouse model of EGFR-driven adenocarcinomas have implicated hyperactivation of the PD-1-PD-L1 axis in tumor immune escape and malignant progression (45–47), and manipulation of Treg generation driven by this axis constitutes one of the most predominant mechanisms of NSCLC occurrence (Figure 1B). The gene discussed is EGFR; the disease is non-small cell lung carcinoma.