Recent genome-wide association studies (GWAS) have highlighted several genetic alterations as predictive risk factors of rapid fibrosis progression in chronic hepatitis C. A single nucleotide polymorphism (SNP) located near interleukin 28B (IL28B) that encodes type III interferon λ3 was strongly associated with interferon-induced clearance of HCV[4,5,6,7,8]. The gene discussed is IFNL3; the disease is chronic hepatitis C virus infection.