Glioblastoma, a highly aggressive brain tumor, poses a formidable challenge due to factors such as angiogenesis, diverse mutations, and evasion of apoptosis. Nitric oxide (NO) plays multifaceted roles in physiological processes, including vasodilation, blood pressure regulation, neurotransmission, and immune response. In the context of glioblastoma, understanding the interaction between NO and tumor cells is crucial. Our study utilizes human and mouse glioblastoma stem cells to investigate how NO influences cell proliferation.We modulate NO activity by either enhancing (using SNAP) or inhibiting (using LNAME) nitric oxide synthase, the enzyme responsible for NO synthesis. Through various staining techniques such as EdU and Ki67, we assess cell division to determine the impact of NO on the proliferation of these tumor stem cells. Preliminary results indicate that inhibiting nitric oxide synthase leads to a significant reduction in cell proliferation.These findings suggest a potential avenue for therapeutic intervention in glioblastoma, highlighting the intricate role of NO in the regulation of tumor cell division. Further investigations will delve into the molecular mechanisms underlying this phenomenon, paving the way for novel strategies in the treatment of this challenging malignancy.