In lung adenocarcinoma, preclinical studies in an EGFR-driven mouse model showed that activation of the EGFR pathway induced PD-L1 expression and recruitment of an increased number of PD1+ and Foxp3+ regulatory T cells that suppressed effector T-cell function to evade host immune response, suggesting that ablating this immunosuppressive response may augment response to therapy.35 Phase-1 clinical trials combining EGFR TKI or ALK inhibitor with anti-PD1 or anti-PD-L1 in EGFR-mutated cancer and ALK-rearranged NSCLC are planned or ongoing (clinicaltrials.gov; NCT02088112; NCT02511184). This evidence concerns the gene EGFR and non-small cell lung carcinoma.