Consistent with previous reports showing that UL10 deletion significantly reduces PRV plaque size, penetration kinetics [5, 40] and pathogenicity [41], this study elucidates the detailed molecular mechanism by which PRV gM induces apoptosis at the late stage of infection to enhance the replication and pathogenicity of PRV in vitro and in vivo, providing an important target for the development of vaccines and treatment of herpesvirus infection-related diseases. The gene discussed is PPP1R3A; the disease is infection.