Nathanson et al. observed, through single-cell analysis of models and clinical samples from patients with glioblastomas treated with EGFR tyrosine kinase inhibitors (TKIs), that tumor cells reversibly upregulated or inhibited the expression of extrachromosomal DNA EGFRvIII, resulting in a different cell phenotype with the best growth trade-off. This evidence concerns the gene EGFR and neoplasm.