Briefly, in response to RSV infection, lung macrophages, peritoneal macrophages, and macrophage cell lines all initiate an early and robust M1 proinflammatory response that peaks at ~8 h, followed by production of endogenous IL-4 and IL-13 that, in turn, drives a strong M2 response peaking at ~48 h post-infection and coincides with expression of PPARγ, a transcription factor that heterodimerizes with RXR and is required for induction of M2 macrophages (19–22). The gene discussed is PPARG; the disease is infection.