They also confirmed that influenza infection could upregulate ANGPTL4 expression level through a STAT3-mediated mechanism, which is consistent with Xu et al.’s findings [42], and STAT can be activated by interferon-gamma (IFN-γ) and interleukin 6 (IL-6) through viral infection triggering host responses. The gene discussed is SOAT1; the disease is viral infectious disease.