In conclusion, overexpression of TL1A in myeloid cells could accelerate the process of hepatic fibrosis, worsen the liver function, promote macrophages recruitment, upregulate the levels of PDGF-BB, TNF-α, and IL-1β in liver tissues and macrophages, and further stimulate the activation and proliferation of HSCs. The gene discussed is IL1B; the disease is Hepatic fibrosis.