Specifically, ATF4 promotes glutamine uptake and utilization by upregulating glutamine transporters (e.g., SLC1A5/ASCT2) and metabolic enzymes (e.g., GLS), enhancing glutamine dependency under metabolic stress (The GLS1 inhibitor IPN60090 enhances antitumor immune response through metabolic reprogramming of T cells and impacts on the tumor microenvironment). This evidence concerns the gene GLS and neoplasm.