CDKN1A and Zika virus infectious disease: This is consistent with a previous report in which ZIKV infection of hiPSC-NPCs resulted in post-transcriptional changes, FOXG1 downregulation, upregulation of apoptotic signaling, and downregulation of cell-cycle pathways, in agreement with FOXG1 role in preventing apoptosis and maintaining CDKN1A-mediated proliferation (Jiang et al., 2018).