Once cells are infected, the mRNA and protein levels of DYRK4 are increased, and DYRK4 acts as a scaffold protein to recruit more TRIM71 and LUBAC to IRF3, increasing IRF3 linear ubiquitination, maintaining IRF3 stability and activation during viral infection, and promoting the IRF3-mediated antiviral response (Fig. 9). This evidence concerns the gene IRF3 and viral infectious disease.