Host resistance to UTI is controlled by innate immunity and there are genetic differences in innate immune responses between patients prone to severe, symptomatic infections and those who develop ABU, affecting the IL-8 receptor CXCR1, the IRF3 transcription factor and in TLR4 promoter sequences [38], [39], [40]. The gene discussed is CXCR1; the disease is bacterial urinary tract infection.