Activation of innate immunity due to the detection of viral replication products in the cell leads to the expression of hundreds of antiviral genes that controls the spread of the infection [12] . The inhibition of different steps implicated in these molecular pathways by viruses has been a matter of extensive study for several years. It has been demonstrated by others and by our group that DENV can inhibit both the production and signaling of type I IFN by the expression of viral proteins. In this way, DENV can mitigate the immune response induced by the host upon infection [24, 25, 29] . Here we have identified the human adaptor molecule STING as a protein with a predominant role in the recognition of DENV by the innate immune system. This adaptor protein was described to reside in the ER, a cellular organelle intimately related to the DENV replication process. Also, STING has been described as part of the TRAP (translocon associated protein) complex that can associate with RIG-I and IPS-1, two proteins with relevant roles in viral detection [41] . Ishikawa et al. also described an inhibition of the STING mediated IFNb production by the yellow fever virus (YFV) NS4B [42] . However, when we tried to replicate these results using the DENV NS4B, this viral protein was unable to decrease the induction of luciferase mediated by STING in an IFNb promoter assay (data not shown).