Due to its mutual suppression of both Th1 and Th2 responses, i.e., high IFN-γ levels inhibit IL-4/STAT6 signaling, whereas high levels of IL-4 suppress the IFN-γ/STAT1 pathway [12], IFN-γ-induced SOCS1 production could increase the threshold of T cell responsiveness to IL-4 [4], thereby facilitating the establishment of a Th1/IFN-γ-biased immune environment during influenza infection [13]. This evidence concerns the gene IL4 and influenza.