It is supported by studies on obesity-induced asthma as follows: (i) obesity on its own increases both ILC2 and ILC3 responses in the lungs (71); (ii) obesity-induced AHR requires IL-17-producing ILC3s (69); and (iii) when obese mice are exposed to ozone [which on its own induces airway inflammation in an IL-33-ILC2-dependent manner (116)], their AHR is amplified via a mechanism mediated by IL-13-producing ILC2s (117). This evidence concerns the gene IL13 and asthma.