A Cell & Bioscience study identifies adenylate kinase 2 (AK2) as a therapeutic vulnerability in gliomas and reports venetoclax as a potent inhibitor candidate. The research, led by Hanwen Lu and Zhanxiang Wang, links AK2 overexpression to higher tumor grade and worse prognosis in clinical specimens. Functional work showed that silencing AK2 suppresses proliferation, induces apoptosis, and inhibits tumor growth in orthotopic mouse models. The study also connects AK2 to an immunosuppressive microenvironment and immune checkpoint-associated patterns, including links to M2 macrophage colocalization. Using structure-based virtual screening, the researchers found venetoclax as the most active AK2 inhibitor candidate. They report mitochondrial-dependent apoptosis and anti-glioma effects with venetoclax across in vitro and in vivo settings, while also stating the data do not establish direct AK2 targeting by venetoclax. For glioblastoma and broader CNS oncology efforts, the AK2–venetoclax pairing adds another repurposing direction and a potential biomarker concept tied to sensitivity.