For example, constitutive activation of XBP1 in tumour-associated DCs (tDCs), driven by lipid peroxidation byproducts, has been found to induce a triglyceride biosynthetic program, which leads to abnormal lipid accumulation and subsequent inhibition of the capacity of tDCs to support antitumour T cells [94] (Fig. 3). Here, XBP1 is linked to neoplasm.