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Introduction Arteriovenous shunting has been described in glioblastoma multiforme (GBM), also known as WHO grade 4 astrocytoma. This case report demonstrates the diagnostic dilemma of GBM, which was subsequently found to have macrovascular arteriovenous shunting. The lesion was initially treated as an ischemic stroke for months. Methods A 65‐year‐old‐man with a past medical history of hypertension, hyperlipidemia, and diabetes presented to a community hospital in February 2023 with worsening left‐sided weakness. The patient started having left‐sided weakness around December 2023, but no work‐up had been completed. The exam was notable for spastic hemiparesis. Results At the time of initial presentation, a non‐contrasted head computed tomography (NCHCT) was interpreted as normal. Magnetic resonance imaging (MRI) of the brain showed diffusion restriction and fluid attenuated inversion recovery (FLAIR) hyperintensity in the right corona radiata and was interpreted as a subacute right corona radiata and gangliocapsular infarct. Computed tomography angiogram (CTA) of the head and neck was unremarkable. He was discharged on aspirin and a high‐intensity statin. He re‐presented in April 2023 with sepsis and was found to have multiple pressure ulcers; his left‐sided weakness had worsened despite a course of inpatient rehabilitation. A repeat NCHCT demonstrated hyperdensity within the suspected infarct, interpreted as hemorrhagic transformation. The next day, he was found to be difficult to arouse and dysarthric. He was subsequently transferred to our institution for further management. On arrival, a CTA of the head and neck was performed, which suggested that the previously described hyperdensity was possibly a venous varix, and a thrombosed developmental venous anomaly or arteriovenous malformation was suggested. The patient then underwent an MRI brain with and without contrast, which noted that there was an increase in size of a heterogeneously enhancing mass centered in the posterior right basal ganglia/corona radiata with extension into right thalamus, right cerebral peduncle, and posterior right body of corpus callosum. The MRI findings were most consistent with GBM. Given the diagnostic uncertainty, the patient underwent a cerebral angiogram, which demonstrated a hypervascular posterior right basal ganglia mass with arteriovenous shunting from the middle cerebral artery to the internal cerebral veins. Shortly after, the patient underwent a brain biopsy, which demonstrated GBM (IDH‐wildtype, WHO grade 4). The patient was ultimately transitioned to hospice. Conclusion This case highlights the presence of macrovascular shunting in GBM. Intratumoral arteriovenous shunting in GBM has been described, and when present, can lead to delay in treatment due to the broadened differential diagnosis. This patient was first treated for an ischemic stroke with subsequent hemorrhagic transformation. Further imaging suggested a venous varix, thrombosed developmental venous anomaly, or arteriovenous malformation, but the combination of the cerebral angiogram and MRI led to the definitive diagnosis in a patient with a short survival period.