We read with interest the Matsuura et al1 genome-wide association study (GWAS) of 456 Japanese patients identifying tolloid like 1 (TLL1) as a novel susceptibility locus for hepatocellular carcinoma (HCC) after clearance of hepatitis C virus (HCV) with interferon-based treatment. Although detailed functional mechanisms were not defined, the authors suggested that the TLL1 rs17047200 single nucleotide polymorphism or other intronic variants in strong LD may influence splicing, resulting in production of a catalytically more active short isoform (TLL1 isoform 2).