By applying a gene expression assay being specific for IFNL3 and discriminating the highly homologous paralogue IFNL2, we demonstrate a lack of an activation of hepatic IFNL3 gene expression in clinical liver biopsy samples from patients with chronic hepatitis C when compared to liver-healthy individuals, patients with liver diseases of non-viral etiology, or patients with chronic hepatitis B. This result complements own previous findings on the lack of hepatic IFNL2/3 gene activation in chronic HCV infection in comparison to non-viral liver diseases in man [17]. Here, IFNL2 is linked to chronic hepatitis B virus infection.