Moreover, in ATF6 knockout MEF cells, phosphorylation of eIF2α, downstream CHOP activity, and Jak–STAT1 phosphorylation induced by IFNα are upregulated upon infection, which implies that virus-induced ATF6 activation is a prosurvival mechanism required for replication and inhibition of the antiviral signaling pathway (Ambrose and Mackenzie, 2013). The gene discussed is ATF6; the disease is infection.