HCMV-infected THP-1 monocytes show higher IFN-β secretion and increased accumulation of phosphorylated IRF3 than do THP-1 derivatives lacking cGAS or STING (16), indicating that the cGAS/STING/TBK1 pathway also contributes to the IFN response to latent HCMV infection within an incompletely differentiated myeloid cell type. This evidence concerns the gene IFNA1 and cytomegalovirus infection.