The demonstration that EGF and FGF2 help retain FOXG1 nuclear localization following ZIKV infection, and that ZIKV induces FGF2 expression supports the combinatorial or dose-dependent role of GFs in forebrain shaping, the pathophysiological relevance of FGF2, and suggests a further role of GFs in ZIKV spread. The gene discussed is EGF; the disease is Zika virus infectious disease.