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The endoplasmic-reticulum (ER) stress response represents a pivotal cellular process, triggered by a variety of stimuli implying incorrect protein folding in the ER. Solid evidence implicates ER stress-induced dysfunction as major contributors in many cancers, among which brain cancers. In this work, an integrative analysis in two transcriptomic datasets scrutinizes the regulatory potency of ER stress mechanisms in glioblastoma. Besides confirming the results of the initial analyses, the integration of both datasets manages to study the effect of cellular stress in conjunction to the dysregulation of the IRE1α branch of the ER stress signaling pathways. Given the respective diversified phenotypic profile of glioblastomas, ranging from increased proliferation to enhanced migration and aggressiveness as a result of the IRE1α molecular switch, this study suggests potential target groups of master regulators of the ER stress pathways, through the application of an established, exhaustive computational framework.