Such regulation is achieved by the elimination and reemergence of EGFRvIII from eccDNA.43 It provided theoretical foundations for pulsed intermittent treatment with higher EGFR TKI doses in GBM patients to achieve better therapeutic outcomes, as extrachromosomal EGFRvIII DNA levels rapidly rise during the treatment interval. The gene discussed is EGFR; the disease is glioblastoma.