Eisenhardt [37] demonstrated that the CXCR3+CD56bright phenotype is a subgroup of NK cells with antifibrotic potential demonstrating a strong killing effect on HSCs and abnormal activity in hepatitis C. Choi [38] found that the activation of mGluR5 in NK cells alleviated liver fibrosis by increasing cytotoxicity and IFN-γ production. The gene discussed is GRM5; the disease is hepatitis C virus infection.