Phenotypically, resistant C5-sufficient C57BL/6J mice die late in infection due to high kidney fungal loads, and associated strong neutrophil-driven inflammatory response at that site, while C5-deficient A/J mice succumb within 24 hrs of infection with little kidney damage, but displaying an allergic-like response associated with high levels of circulating TNFα, IL-6, MCP-1, MCP-5 and eotaxin[20], [21], resulting in multiple organ failure including cardiomyopathy[21]. The gene discussed is CCL2; the disease is infection.