Recent, studies of experimental Sendai virus infection in murine embryo fibroblasts revealed new molecular mechanisms by which NF-kB signaling components (p50 and p65 subunits) are recruited to the cell nucleus (see Figure 2) to directly activate and up-regulate both Cyclin G1 (CCNG1) and p21 (CDKN1) at the level of gene expression, enhancing the transcription of both genes upon virus infection (Burns and Kerppola, 2022). The gene discussed is NFKB1; the disease is viral infectious disease.