Compared to other clinically available dual CDK4/6 inhibitors, abemaciclib exhibits increased blood–brain barrier penetration and CDK4 selectivity and has been shown to achieve therapeutic concentrations in brain tissue.16,17 Notably, patient-derived IDH-mutant glioma cells, including those derived from oligodendroglioma, were recently shown to exhibit decreases in cell viability and proliferation when treated with abemaciclib in vitro, and abemaciclib improved survival in orthotopically implanted IDH-mutant glioma xenograft models.18 Here, CDK4 is linked to glioma.