While STAT2 deficiency alone did not affect Brucella burdens, a combined deficiency of STAT2 and the IFN-γ receptor led to elevated Brucella burdens in brains and blood, and a higher likelihood of developing neurologic symptoms relative to animals lacking the IFN-γ receptor alone.<h4>Conclusions</h4>Our findings indicate that T cells and IFN signaling through both STAT1 and STAT2 play complex and important roles in protecting against bacterial colonization and development of neurologic symptoms following infection by Brucella. The gene discussed is STAT1; the disease is infection.