In these studies, the mortality from influenza pneumonia and secondary bacterial pneumonia infection in the transgenic mice that overexpress GM-CSF only in the lung was 0% compared to 100% in wild-type mice [2] and alveolar macrophages (AMs) were the major mediators of SPC-GM mice resistance that overexpress GM-CSF only in the lungs under the control of the human SP-C promoter [2–4]. Here, CSF2 is linked to influenza.