A previous study found that high PD-L1 expression in NSCLC patients with mutant EGFR was associated with de novo resistance to EGFR-TKIs (tyrosine kinase inhibitors).[26] Our study showed that the majority (86.4%) of observed EGFR mutations were accounted for by exon 19 deletions and exon 21 L858R substitutions. This evidence concerns the gene CD274 and non-small cell lung carcinoma.