ZIKV infection of human monocytes has also been shown to activate TLR2 signaling, leading to NF-κB activation and a strong NF-κB-dependent pro-inflammatory response, with increased production of TNFα, IL-1β, IL-6 and IL-10 in ZIKV-infected monocytes, which may be involved in the control of ZIKV proliferation. The gene discussed is TNF; the disease is Zika virus infectious disease.