It is possible that in patients with donor rs368234815 TT/TT genotype, decreased expression of ISGs is associated with increased progression to fibrosis in the setting of recurrent hepatitis C. Conversely, IFNL3 polymorphisms have been shown to be associated with etiology-independent hepatic fibrosis, suggesting that the mechanism underlying the association between IFNL4 TT/TT genotype and post-transplant fibrosis might be HCV-independent [15]. The gene discussed is IFNL3; the disease is hepatitis C virus infection.