Mechanistically, glutamine is a major precursor for glutathione synthesis, therefore, limiting the utilization of glutamine by tumor cells leads to the reduction in GSH, inhibits the activity of sarcoplasmic reticulum Ca2+-ATPase (SERCA), and activates the NF-κB signaling pathway, thereby promoting the expression of tumor PD-L1 and inactivating the co-cultured T cells. The gene discussed is NFKB1; the disease is neoplasm.