We raise the hypothesis that the early burst of TGF-β1 down-modulates inflammation in AGMs, whereas the long lasting plasma TGF-β1 levels reflect the inability of MACs and humans to resorb virus-driven inflammation and activation [1], perhaps because HIV/SIVmac infections would render cells unresponsive to TGF-β1. The gene discussed is TGFB1; the disease is infection.