Moreover, the invasion and metastasis associated with tumor-derived small extracellular vesicle (sEV) PD-L1 could be avoided because autophagy activation via temsirolimus (TEM), an FDA-approved anticancer drug, suppressed the cellular PD-L1 levels and PD-L1 levels in sEVs in a dose-dependent manner in cellular models of breast cancer [138]. This evidence concerns the gene CD274 and breast carcinoma.