Additionally, the loss of phosphatase and tensin homolog (PTEN) activates the phosphatidylinositide 3-kinase/Akt (PI3K/Akt) and mammalian target of rapamycin (mTOR) pathways, which leads to upregulation of PD-L1 on glioma and breast cancer cells [23,24]. This evidence concerns the gene AKT1 and breast carcinoma.