Continually, Jia and co-workers found that MLN4924-induced neddylation inhibition caused the accumulation of ATF3 to promote prosurvival autophagy by regulating NF-κB-Catalase-ROSATF3 axis in esophageal cancer cells, suggesting inhibition of ATF3-mediated autophagy as a promising strategy to improve neddylation mediated ESCC treatment 120. The gene discussed is ATF3; the disease is esophageal cancer.