For instance, it can upregulate the expression of programmed‐death ligand 1 (PD‐L1), facilitating immune evasion in cancer cells.[23] Furthermore, cholesterol induces CD8+ T cell exhaustion via an endoplasmic reticulum stress‐XBP1‐dependent mechanism.[24] Consequently, reducing cholesterol in the tumor microenvironment not only sensitizes cellular ferroptosis but also revitalizes T cell function and reverses tumor immunosuppression,[25] highlighting its significant potential in tumor synergistic ferroptosis‐immune therapy. This evidence concerns the gene XBP1 and neoplasm.