The key advantages of epigenetic drugs lie in their multipathway synergy enabling the coordinated modulation of MYCN signaling and p53 restoration through single-target interventions, bidirectional transcriptional control that simultaneously suppresses oncogene hyperactivation (e.g., ALK, PHOX2B) and reactivates epigenetically silenced tumor suppressors (e.g., CASZ1, CLU), and heritable chromatin remodeling effects ensuring sustained therapeutic outcomes through the stable transmission of modified chromatin states across cell divisions. The gene discussed is MYCN; the disease is neoplasm.