Here, we demonstrate that LAG3 affects CD4+ T cells to participate in the immune tolerance induced by E. multilocularis infection and plays a critical role in long-term infection; LAG3 deficiency affects CD4+ T-cell skewing, promoting a Th1 phenotype and inhibiting Th2 and Treg induction, which strongly suggests that blocking LAG3 could be a strategy used in future clinical treatment of patients with AE. The gene discussed is CD4; the disease is infection.