For instance, Meng et al.'s studies revealed that IL-17A exacerbate hepatic fibrosis by focus on how inflammatory cells respond to the changes of IL-17A signaling in response to liver injury; whereas our study confirmed that IL-17A promoted hepatic fibrogenesis by focus on how the intracellular autophagy activity is regulated by the activation of IL-17A signaling in response to liver injury. The gene discussed is IL17A; the disease is Hepatic fibrosis.