In addition, they observed that IL-33 polarized M2 macrophages to produce IL-13 and induced the expansion of ILC2s to produce IL-13, whereas we report IL-4 and IL-5 but no IL-13 production suggesting a predominant role of M2 macrophages rather than ILC2 in enhancing profibrogenic cytokine production in an ST2- and macrophage-dependent manner and leading to lung fibrosis. The gene discussed is IL33; the disease is pulmonary fibrosis.