Moreover, previous studies have demonstrated that immune inhibitory receptors [e.g., programmed cell death protein-1 (PD-1), T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT)] participate in the dysfunction and imbalance of T-cell subsets during chronic E. multilocularis or hepatitis B virus (HBV) infection to maintain immune tolerance, thus accelerating disease progression [6,9–12]. The gene discussed is PDCD1; the disease is Hepatitis.