Virus‐infected liver cells and HCC cells evade immunosurveillance by upregulating PD‐L1 expression on their surface, which interacts with T‐cell immune checkpoint receptors, including B‐ and T‐lymphocyte attenuator (BTLA), PD‐1, and CTLA‐4, inhibiting T‐cell activation and immune responses, enabling malignant cells to escape immune detection, proliferate uncontrollably, and accelerating the progression of viral hepatitis to HCC [588]. The gene discussed is CTLA4; the disease is hepatocellular carcinoma.