PD‐L1 overexpressed on tumor cells can bind to PD‐1 on the activated T‐cell membrane, promoting tyrosine phosphorylation in the immune‐receptor tyrosine‐based switch motif (ITSM) domain of PD‐1, leading to the dephosphorylation of downstream protein kinases, Syk and PI3K, which then inhibit the activation of downstream AKT, ERK, and other pathways.16, 17. This evidence concerns the gene CD274 and neoplasm.