We think that the possible causes of this difference are mainly explained by the following differences in the models of liver fibrosis: first, there are differences in the amount of TNF-α secretion, and in our model, 40 ng/ml TNF-α promotes apoptosis; second, TNF-α causes the activation of different downstream signaling pathways, and in our model, TNF-α mainly stimulates the activation of the TNF-R1/caspase 8 pathway, not the NF-κB signaling pathway. The gene discussed is CASP8; the disease is Hepatic fibrosis.