A glioma study characterized adenylate kinase 2 (AK2) as overexpressed with tumor grade and poor prognosis associations, then identified venetoclax as a potent candidate inhibitor in multi-omics and functional experiments. AK2 silencing suppressed proliferation and induced apoptosis, and in orthotopic mouse models it inhibited tumor growth. The research also links AK2 to immunosuppressive microenvironment features and proposes venetoclax sensitivity hypotheses—while stopping short of proving direct AK2 targeting. The signal supports AK2 pathway exploration as a therapeutic vulnerability and adds another repurposing-style angle for difficult-to-treat brain tumors.