SOCS3 functions as a negative immune regulator and demonstrates differential regulation patterns across viral infections: HSV-1 upregulates SOCS3 via STAT3 activation to suppress JAK/STAT antiviral signaling [24]; influenza A virus induces SOCS3 through an NF-κB-dependent pathway to attenuate type I interferon responses [25]; while HIV-1 downregulates SOCS3 to trigger persistent immune activation that promotes viral replication [26]. The gene discussed is SOAT1; the disease is viral infectious disease.