Since the Jak-STAT pathway is a key modulator of the interface between host immunity and viral infection [18], we sought to use supraphysiological concentrations of ruxolitinib as a tool to understand the blockade of Jak-STAT signaling and subsequent production of ZIKV infection in clinically relevant cells including primary human HC, trophoblasts, and neuroblastoma cells. The gene discussed is SOAT1; the disease is viral infectious disease.