In summary, there is a clear link between IFNL gene SNPs and HCV treatment outcome as well as spontaneous clearance.
The overlapping response of IFN-alpha and IFNL signaling on the one hand and the tissue specificity of the IFNLR on the other hand made IFNL promise that the replacement of IFN-alpha by IFNL would yield the same therapy outcome with fewer side effects.
IFNL3 has the highest activity among the IFNL types and therefore might be more suitable as therapeutic agent than IFNL1 .
For instance, hepatitis E virus is sensitive to IFNL in in vitro models  and currently treatment options for hepatitis E are limited.
Chinnaswamy, "Gene-disease association with human IFNL locus polymorphisms extends beyond hepatitis C virus infections," Genes and Immunity, vol.
Caption: Figure 1: Sequence alignment and amino acid conservation of IFNLs. Clustal Omega (1.2.3) alignment  of IFNL proteins (IDs: Q8IU54, Q8IZJ0, Q8IZI9, and K9M1U5).
Caption: Figure 4: Schematic representation of the IFNL chromosome locus.
All four IFNLs are encoded on chromosome 9 in the 19q13.13 region.
These findings suggest a common ancestor gene for all IFNLs .
Signaling in response to IFNLs is initiated by dimerization of the two IFNLR subunits.
Antiviral effects of IFNLs are largely shared with type I IFNs.