Despite Rag1-/-Rorcgfp/gfp mice exhibiting a lack of ILC3s (another source of IL-17) and having similar pathogenic outcomes in IL-33 induced lung inflammation (75), IL-17-producing ILC3s can still play an important role in different disease contexts such as obesity-induced asthma in which they can mediate the development of airway hyperreactivity and thus, should be at the forefront when considering IL-17-producing ILC populations (74). This evidence concerns the gene IL17A and obesity due to melanocortin 4 receptor deficiency.