In line with a previous report (20, 62, 63), our findings suggest that PEDV may exploit kinase-dependent pathways, such as MAPK/AP-1 and JNK/p38, via TRAF2, TRAF6, and TBK1 to enhance viral replication during the acute phase of infection in weaned piglets, whereas such modulation was absent in newborn piglets. The gene discussed is TBK1; the disease is infection.