Glioblastoma is the most lethal form of primary brain tumour. Standard treatment combines debulking surgery, radiotherapy and temozolomide chemotherapy but is of limited efficacy, producing a median survival time of only ~15 months. Glioblastoma is not responsive to checkpoint inhibitors and there have been no meaningful improvements to treatment in decades. Accordingly, there is much interest in developing novel therapies based on immune targeting of glioblastoma. The success of these approaches, however, relies on identification of a target antigen expressed on tumour cells but not healthy tissues. We show here that fibroblast activation protein (FAP) is a candidate for such approaches. FAP is a membrane-bound extracellular protease with limited expression in healthy tissues but elevated expression on fibroblasts involved in tissue remodelling, such as during wound healing or tumour formation. Here, immunohistochemical staining of glioblastoma patient tissue specimens revealed expression of FAP in the majority of tumours examined, whereas adjacent normal brain tissue uniformly lacked expression. FAP was detected in both the main tumour parenchyma and in a distinct perivascular pattern. These results are supported by analysis of RNA sequencing and microarray data from The Cancer Genome Atlas (TCGA), which showed significantly elevated levels of FAP gene expression in glioblastoma specimens compared to normal brain tissue. A panel of 15 patient-derived glioma neural stem cell cultures was examined for FAP expression by flow cytometry, revealing that the majority (10/15) expressed some level of cell surface FAP. This finding reveals that, in contrast to epithelial cancers where FAP expression is limited to stromal fibroblasts, the cancer cells themselves may express FAP in glioblastoma. Together, these data reveal FAP as a potential candidate for targeted immunotherapy approaches in glioblastoma.