Inflammatory diseases of the lung are a major cause of morbidity and mortality. Allergic lung inflammation often stems from the overproduction of type 2 cytokines. The resulting type 2 inflammation is frequently caused by an inappropriate immune response to relatively harmless allergens and often associates with asthma. Until recently, the primary contributors of type 2 cytokines were believed to be T helper (Th) 2 cells. This concept was challenged by the discovery of group 2 innate lymphoid cells (ILC2s) in the lung, which represent a major source of type 2 cytokines during the acute inflammatory phase. Recent advances in our understanding of the regulation and development of ILC2 have redrawn the roadmap of type 2 inflammation. Indeed, ILC2s appear to be critical for the induction of adaptive immunity and, thus, play a central role for immune regulation. As one of the first responders in the entire Th2 cascade, ILC2 might serve as the early tile in a Th2 domino effect. As such, ILC2s present an attractive target for future drug development.