We chose to examine the liver for this analysis for several reasons: 1) infection appears to induce a novel ILC1-like subset that is common to the liver and spleen; 2) the liver contains ILC1s under steady-state, allowing for direct comparison of steady-state ILC1s and T. gondii-induced ILC1-like cells; and 3) the infected liver uniquely contains a Tbx21-/- Eomes+ CD49a+ population. This evidence concerns the gene ITGA1 and infection.