The consequences of this functional interplay are twofold: On one hand, the NS5−hSTAT2 interaction may facilitate the proteasome-mediated degradation of hSTAT2, thereby influencing host immune response; on the other hand, it also leads to the inhibition of NS5-mediated RNA synthesis during the early stages of infection, which underscores the delicate balance between viral replication and immune evasion. The gene discussed is RAF1; the disease is infection.