ISX transcriptionally regulated the downstream indoleamine 2, 3‐dioxygenases (IDOs), thereby dysregulating tryptophan catabolism and enhancing the levels of immune checkpoint regulators (PD‐L1 and B7‐1) and epithelial–mesenchymal transition (EMT) in patients with HCC.[13] Notably, classic IFN‐α or DAA treatment did not inhibit enhanced HCV‐induced ISX‐relevant signaling affecting metabolic disturbance and immune suppression. The gene discussed is CD274; the disease is hepatocellular carcinoma.