Similarly, in prostate and triple-negative breast cancer cells, the Sigma1 activator could upregulate PD-L1 expression by promoting the glycosylation of PD-L1, and the Sigma1 inhibitor could sequester and eliminate PD-L1 by autophagy, thus preventing functional PD-L1 expression at the cell surface [55]. This evidence concerns the gene CD274 and triple-negative breast carcinoma.