Given that IL-33 could regulate metabolic inflammation by engaging ILC2s and activating downstream type 2 immune response [42, 43], we tested circulating levels of Th2 cytokines IL-5/13 and found the distribution trend of IL-5/13 levels in different groups were basically consistent with that of IL-33, indicating that Th2 immune responses were activated during the progression of obesity. The gene discussed is IL5; the disease is obesity due to melanocortin 4 receptor deficiency.