MAVS and viral infectious disease: 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).