This project is testing whether TEAD inhibition, with or without CDK4/6 inhibitor abemaciclib, is an effective therapeutic strategy in patient-derived meningioma organoids and if it is a clinically relevant 3D model of tumor biology. The research focuses on tumors with an NF2 mutation that causes dysregulation of the Hippo pathway through YAP/TAZ–TEAD activation, potentially creating a targeted therapeutic vulnerability. To address this, drug efficacy will be evaluated using viability and proliferation assays in 3D organoid models, followed by IHC staining to assess tumor architecture and cellular context. In parallel, this model system will be used to evaluate how well organoids recapitulate in vivo tumor behavior, supporting their use as a translational platform. Milestones will include the optimization of organoid culture conditions, drug-treatment assays, and quantitative analysis of treatment response. The impact of this work is to advance precision oncology approaches for meningioma by identifying pathway-specific therapeutic strategies and validating organoids as clinically relevant models for treatment testing.