More importantly, the effects of koumine upon mitochondria membrane potential, ROS production, and the phosphorylation of ERK, p38, p65, and IκBα could be significantly reversed by ROS inhibitor, indicating that koumine affects HCC cell fate through producing excess ROS via ERK/p38 MAPK phosphorylation and NF-κB signaling. The gene discussed is NFKB1; the disease is hepatocellular carcinoma.