Recently, both advancement in our understanding of asthma pathogenesis and the clinical success of biologic therapies interfering with type 2 cytokine signaling related to interleukin (IL)-5, IL-4, and IL-13 in severe asthma patients [4,5] have led to the current dichotomy of type 2 and non-type 2 inflammation, which will improve our interpretation of the extremely heterogeneous nature of chronic inflammation in asthma. Here, IL13 is linked to asthma.