Nattermann and colleagues convincingly demonstrated that the ineffective immune response during HCV infection may be directly linked to aggravation of hepatic fibrogenesis, as CD4(+) T cells were shown to stimulate anti-fibrotic NK cell activity via IL-2 mediated upregulation of NKG2D, and an impaired activity of CD4(+) T cells contribute to acceleration of liver fibrosis [35]. The gene discussed is IL2; the disease is Hepatic fibrosis.