Tyrosine kinase inhibitors (TKIs) targeting EGFR have been applied in cancer treatment and have shown considerable efficacy in patients with non-small cell lung cancer, breast cancer, glioma, etc. However, plenty of patients suffer from intrinsic and acquired resistance mediated by EGFR, making PROTAC a promising approach because of its capability to degrade wild-type and multiple mutants simultaneously [28,29]. The gene discussed is EGFR; the disease is glioma.