However, Sp1 overexpression increased basal levels of phospho-IRE1α and cleaved ATF6α and caused a significant reduction in the BA-induced expression of phospho-PREK, phospho-eIF2α, and CHOP proteins, suggesting that Sp1 played critical roles in promoting both the activation of the IRE1α/ATF6α pathways and the inhibition of the PERK/eIF2α/CHOP axis in GBM cells. Here, ATF6 is linked to glioblastoma.