Subsequently, infection with mutant HCMV lacking the two miRNAs induced increased IKKα and IKKβ protein levels, demonstrating an impaired ability to control NF-κB signaling at late stages of lytic infection, and increased production of proinflammatory cytokines compared to the wild-type virus in cell types relevant to HCMV infection in vivo. The gene discussed is NFKB1; the disease is infection.