Based on the observation that patients carrying the unfavourable IL28B genotypes seem to have an inappropriately up-regulated intrahepatic expression of interferon-stimulated genes (ISGs), some authors have hypothesised that those with a favourable IL28B profile, having a lower intrahepatic ISGs expression, may be more sensitive to exogenous IFN and, thus, more likely to respond to treatment and to eradicate the infection (Honda et al. 2010; Urban et al. 2010). Here, IFNL3 is linked to infection.