The lack of absolute ablation of latency upon infection with IκBαM might reflect (i) the utilization of alternative NIK/IKK1-mediated NF-κB activation, (ii) the establishment of virus infection in cell populations that do not rely on NF-κB, and/or (iii) inadequate expression of the IκBαM transgene; the HCMV immediate-early promoter might not drive sufficient levels of IκBαM expression in some cells or cell populations (as such, the residual latency observed at 16 dpi might simply reflect a population of cells in which NF-κB activation was not suppressed). Here, NFKB1 is linked to infection.