In line with these findings, the inhibition of Gln metabolism with V9302 and Bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl)ethyl sulfide (BPTES) in murine syngeneic colorectal carcinoma model increases PD-L1 expression in tumor cells, activates T-cell-mediated Fas cell death signaling, and synergizes with anti-PD-L1 immunotherapy [90]. This evidence concerns the gene CD274 and colorectal carcinoma.