The absence of STAT1, the major proinflammatory signaling pathway for IFNγ, converts the subclinical infection phenotype universally observed with A. phagocytophilum mouse models to one with severe clinical signs (reduced activity, piloerection, crouching, dehydration, and weight loss), dense infiltration of inflammatory cells, and robust proinflammatory cytokine/chemokine responses compared with WT controls (Choi et al., 2014a). The gene discussed is STAT1; the disease is infection.