Approaches may involve identifying and inhibiting “dual-function nodes” like EZH2 or BRD4, which control chromatin structure and metabolic activity; designing combination therapies that pair epigenetic inhibitors (e.g., HDAC or BET inhibitors) with metabolic inhibitors (e.g., LDHA or CPT1A blockers); and employing advanced delivery systems such as hypoxia-responsive nanocarriers or tumor-activated prodrugs to improve treatment specificity and efficacy. The gene discussed is EZH2; the disease is neoplasm.