Hence, complement deficiencies and MyD88 mutations do not appear to confer a significant risk for invasive candidiasis in humans as opposed to mice [26]; however, a recent large cohort study demonstrated that TLR1 single nucleotide polymorphisms in Caucasian patients were associated with heightened risk for development of invasive candidiasis, suggesting that TLR signaling may contribute to optimal anti-Candida immunity in humans [29]. The gene discussed is TLR1; the disease is candidiasis.