Furthermore, the interaction between PD-1 and PD-L1 extends to TAMs in the cervical cancer microenvironment, wherein PD-1's pathway activation may shift TAMs from an anti-tumor M1 phenotype to a pro-tumor M2 phenotype, thereby allowing cancer cells to evade immune detection by expressing PD-L1, thereby muting the immune responses of both TAMs and T cells and promoting tumor progression and dissemination [8–10]. This evidence concerns the gene CD274 and neoplasm.