It could not only induce tumor cell necroptosis and trigger immunogenic cell death by controlling the Gln metabolism inhibitor BPTES, but also remodel the tumor immune microenvironment by increasing M1-like TAM polarization and reducing M2-like TAMs infiltration and T-cell depletion, thereby improving the effectiveness of anti- programmed cell death ligand 1 (PD-L1) immunotherapy. This evidence concerns the gene CD274 and neoplasm.