We then investigated whether increases in EGFR or PI3K signaling caused the increased susceptibility to influenza infection in the absence of Socs5. Wild-type and Socs5−/− mice were treated with either vehicle control (captisol), PI3K inhibitor (BKM-120) or EGFR inhibitor (Erlotinib) followed by infection with H1N1 PR8 virus. The gene discussed is SOCS5; the disease is influenza.