In addition, we propose a bi-directional regulation model of EGFR-amplified glioblastoma: the emergence of neo-loop around oncogenes contributed to the activation of the oncogenic transcription program in A172 (Fig. 6J, left) while disappearing or weakening of existing loop around tumor suppressor crippled the anti-tumor line of defense in HA1800 (Fig. 6J, right). The gene discussed is EGFR; the disease is glioblastoma.