We hypothesized that since KLRG1 expression and the production of IFN-γ by F3 late stage effector CD8+ T cells is IL-12 dependent (Wilson et al., 2008, 2010), CXCR3 expression may also be IL-12 dependent, possibly explaining the attenuation of effector cells to the site of infection in our model. The gene discussed is CD8A; the disease is infection.