In response to influenza infection, innate immunity is activated to produce type I IFNs (IFN-β) in restricting virus replication and spread.10 Stressful experiences could activate the hypothalamic-pituitary-adrenal (HPA) axis, resulting in an elevation of stress hormones, mainly glucocorticoids (GCs) that could induce immunosuppression.11,12 Our previous studies have indicated that stress-provoked host’s susceptibility to influenza was associated with impeding IFN-β response.13,14 However, how stress influences IFN-β response during influenza virus infection needs to be further dissected. This evidence concerns the gene IFNB1 and influenza.