Cultures with MYCN gain (WK029, WK040, WK042, WK042R) or an activating mutation (WK010), showed a significantly stronger sensitivity to BTZ than tumor organoids with wildtype MYCN. The combination of low-dose BTZ and the HDAC inhibitor vorinostat (SAHA) that synergistically induces apoptosis in vitro [40], showed a significant additive effect in organoids with high MYCN expression, particularly in the relapsed case (WK042(R), figure S5). The gene discussed is MYCN; the disease is neoplasm.