Overall, BsAbs targeting NKG2D together with EGFR/ERBB2 re-engineer immune recognition within the TME by bridging engineered NK cells to oncogenic drivers and—when coupled with IL-15-based activation—achieve synergistic effects with broad antigen adaptability, thereby expanding therapeutic options for GBM immunotherapy 85. The gene discussed is ERBB2; the disease is glioblastoma.