This innovative combination potentiated the antitumor activity of ARV825 through multiple mechanisms: (1) Enhanced tumor accumulation and cellular internalization of ARV825 via GLUT1-mediated active targeting; (2) Induction of tumor cell apoptosis through downregulation of Bcl-2 protein mediated by BRD4 protein degradation; (3) Promotion of T cell infiltration and antitumor immune response via BRD4 degradation-mediated PD-L1 suppression combined with GRh2-mediated collagen fiber degradation in the tumor ECM. Here, SLC2A1 is linked to neoplasm.