It has recently been suggested that, during infection with P. brasiliensis, human neutrophils may modulate the adaptive immune system toward a protective response mediated by a T helper 1 (Th1) pattern via Toll-Like Receptor 4 (TLR4) and Dectin-1, inducing interferon- (IFN-) γ production upon stimulation with the combination of interleukin- (IL-) 12 and IL-15 [14]. The gene discussed is TLR4; the disease is infection.