NLRP3 and fungal infectious disease: TRIM31 promotes the catalyzation of K63-linked polyubiquitination of mitochondrial antiviral signaling protein (MAVS), and this modification facilitates MAVS aggregation which further induces Interferon-β (IFN-β) production to inhibit virus replication.34 We also found that TRIM31 can promote proteasomal degradation of NLR Family Pyrin Domain Containing 3 (NLRP3) and therefore inhibits NLRP3 inflammasome activation and attenuates the DSS-induced colitis inflammation.39 Until now, the role of the TRIM family during fungal infection had rarely been reported.