As March1 regulates the display of various transmembrane proteins at the plasma membrane, and given the established proinflammatory role of the complement by-product, C5a, in allergic asthma [36–38], we wondered if March1 could modulate the complement receptor (C5aR; CD88) expression in lung inflammatory cells as potential pathway in modulating allergic reactions. The gene discussed is C5; the disease is allergic asthma.