IκBα is modified by SUMOylation on lysine 21, which blocks its ubiquitination and degradation.50,51 Furthermore, TRIM38 mediates the SUMOylation of cyclic GMP-AMP synthase (cGAS) on K464, which suppresses the K48-associated polyubiquitination and degradation of cGAS and thus ensures an effective innate immune response to DNA viruses during the early phase of infection.52 In our study, the SUMOylation of TAB2 impaired the recruitment of TAB2/TAK1 to TRAF6 and further suppressed the activation of the downstream MAPK and NF-κB signaling pathways. The gene discussed is TAB2; the disease is infection.