Through single-cell analysis of patient-derived models and clinical samples of glioblastoma patients treated with EGFR tyrosine kinase inhibitors (TKIs), researchers have found that EGFR, c-MYC, N-MYC, and others rely on a high level of ecDNA amplification in glioblastoma cells and that loss of ecDNA that encodes EGFRvIII promotes resistance to TKIs. Here, EGFR is linked to glioblastoma.