From these results, we propose that phosphorylation of Grasp65 during HCMV infection, likely by CDK1 and/or, potentially, by PLK1 or ERKs, reduced the capacity of this resident Golgi membrane protein to tether the Golgi cisternae, thus allowing the Golgi membranes to fragment during AC morphogenesis. Here, GORASP1 is linked to cytomegalovirus infection.