Our previous study indicated that NJXA also showed tumor inhibitory effects via the down-regulation of heterogeneous nuclear ribonucleoprotein K (hnRNPK) by accelerating ubiquitin-proteasome-dependent hnRNPK degradation, which then induced cell cycle arrest through the c-Myc-cyclin/Cdk-Rb-E2F1 pathway. The gene discussed is E2F1; the disease is neoplasm.