Although it has been reported that KSHV infection is also sensed by the cGAS-STING pathway and this pathway regulates the reactivation of KSHV from latency (Ma et al., 2015; Zhang et al., 2016), a recent report has shown that STING signaling is not critical in KSHV latent infection, replication, or in its spread after lytic reactivation in endothelial cells (Vogt et al., 2020). The gene discussed is STING1; the disease is disease arising from reactivation of latent virus.