The observation that TLR3 activation by ZIKV induces proinflammatory cytokines at the expense of the IFN response, along with data showing robust activation of a TLR3-dependent immune response in hNPCs after poly(I·C) stimulation (40), led us to investigate whether TLR3 signaling might suppress the IFN response upon ZIKV infection in neural progenitor cells. The gene discussed is TLR3; the disease is Zika virus infectious disease.