The recent epidemic of ZIKV infection in South America and parts of Asia has spurred widespread interest in ZIKV infection and pathogenesis, and it is now known that ZIKV infects cells through the entry receptor AXL and causes the activation of Toll-like receptor 3 (TLR3), and consequently, the infection causes attenuated neurogenesis, dysregulated cell cycle, and increased cell apoptosis in hNPCs [6–8]. The gene discussed is TLR3; the disease is infection.