In ovarian cancer, XBP1, which is promoted by lipid peroxidation byproducts, is activated to induce tumor-associated DC (tDC) to initiate triglyceride biosynthesis procedures, leading to abnormal lipid accumulation and subsequently inhibit tDC’s ability to support anti-tumor T cells, thereby achieving the purpose of inactivating anti-tumor immunity and promoting tumor development (44). This evidence concerns the gene XBP1 and ovarian cancer.