Gliomas are malignant tumours arising from glial cells in the brain and are some of the most aggressive forms of tumours with high mortality rate. Beyond intense multimodal therapies, the median rate of survival is only 15 to 16 months. Thus, there is a dire need for better therapies. In the brain tumour microenvironment, glioma-associated microglia/macrophages are reported to interact with the tumour, suggesting a role of innate immunity in brain tumour progression. AIM2 is an inflammasome forming innate immune receptor that detects cytosolic double stranded DNA. Recently, AIM2 is found to have emerging roles in many tumour types, including; breast, ovarian and colorectal cancer. Except for a preliminary in vitro study showing that glioblastoma primary cultured cells and cell lines express 88.4% and 93.0% of non-spliced and spliced AIM2, respectively, there is no report showing the link between AIM2 and glioma. Thus, deciphering the link between AIM2 and gliomas might pave way for effective therapies to treat gliomas. As an initial step, the aim of this thesis is to characterize the expression pattern of AIM2 in Glioma. Upon gene expression analysis through fluorescence immunohistochemistry staining and PCR, it is found that AIM2 expression is upregulated in gliomas. This opens up new directions to further explore the role of AIM2 in glioma in an aim to design novel effective therapeutic interventions for glioma. Nevertheless, this is a preliminary yet important study as the whole AIM2 inflammasome signaling pathway needs to explored in the specific cell populations of glioma