However, significantly decreased production of IFN-γ was a specific finding in the CXCR3(+)CD56Bright subset, suggesting that CXCR3(+)CD56Bright NK cells might represent a NK cell subset with dys-regulated anti-fibrotic potential in chronic hepatitis C. As a potential mechanism underlying this impaired functional activity we found chronic hepatitis C to be associated with a significantly decreased surface expression of NKG2D (Figure 5C). Here, KLRK1 is linked to chronic hepatitis C virus infection.