Here, we show that the HCMV UL138 protein, which is expressed during latency (27), inactivates the cGAS/STING/TBK1 pathway and during infection reduces the accumulation of the mRNA for IFN-β in both highly differentiated fibroblasts permissive for HCMV productive replication and incompletely differentiated myeloid cells (THP-1 monocytes and primary CD34+ HPCs) that support HCMV latency. The gene discussed is STING1; the disease is infection.