After XBP1 is silenced under hypoxic conditions, tumor growth and survival decline, suggesting that XBP1 is a key component of cell survival.35 XBP1 is more highly expressed in glioma tumors than that in normal tissues and knocking out XBP1 can increase cell death under stress conditions.36 Studies show that XBP1 silencing reduces the viability and tumorigenicity of glioma cells by inhibiting expression of exocrine kinase II (HK2).37 In colon cancer, β-catenin inhibits XBP1s-mediated enhancement of HIF-1α target gene expression. Here, HK2 is linked to neoplasm.