SMURF1 was then recruited to PRMT7 in a MAVS-dependent manner to catalyze the K48-linked polyubiquitination of PRMT7 to ensure its timely proteasomal degradation and subsequent RIG-I-MAVS activation, while SMURF1 degraded MAVS, TRAF3, TRAF6, or USP25 in later viral infection stages to avoid excessive RLR signaling activation (146). This evidence concerns the gene PRMT7 and viral infectious disease.