Neonates responded to antigens with more IL-10 which could be reversed via TLR stimulation restoring a robust pro-inflammatory profile and TH1 response to vaccines.83–86 Furthermore, infants produced weaker pro-inflammatory responses involving IL-12, TNF-α, and IL-β thereby enhancing susceptibility to tuberculosis.87 Polymorphisms in the TLR-1/2/6 pathway were also proposed to affect the efficacy of BCG since infants of tuberculosis endemic countries routinely received this vaccine.88,89. The gene discussed is TLR1; the disease is tuberculosis.