Actin disruption releases NOD2 from cytoskeleton structures and increases NF-κB activation and IL-8 secretion (Figure 2g), indicating that the recruitment of NOD2 in Rac1-induced dynamic cytoskeletal structures may represent a strategy to prevent the NF-κB signaling in uninfected cells and to rapidly activate NOD2 during bacterial infection [59]. The gene discussed is NFKB1; the disease is bacterial infectious disease.