For mutant EGFR, preclinical studies indicate its potential to enhance PD-L1 expression within tumors via pathways such as PI3K-AKT mTOR, Hippo YAP, and IL6-JAK-STAT3, thus providing a theoretical basis for considering PD-1/PD-L1 inhibitors in EGFR-mutant NSCLC [6,7]. This evidence concerns the gene CD274 and non-small cell lung carcinoma.