Indeed, tissue-resident ILC2s have been shown to produce IL-4 and IL-13 that sustain AAMs for the establishment of inflammatory thresholds in neonate and adult lungs,49 and in adipose tissue to protect from obesity.50 Such an environment may be maintained through tissue-resident macrophages self-renewing and proliferating in response to IL-4 without additional recruitment.51 This evidence concerns the gene IL13 and obesity due to melanocortin 4 receptor deficiency.