To determine whether the Ser468 phosphorylation of RelA is necessary for its degradation, we established Mavs+/+ MEFs that stably express the RelA variant carrying the Serine 468-to-Alanine mutation (RelA.S468A) or wild-type RelA by lentivirus infection, and assessed RelA ubiquitination in γHV68-infected MEFs. Here, MAVS is linked to lentivirus infection.