Remarkably, adoptive transfer of Atg5−/− ILC2 cells attenuated IL-33-induced pulmonary inflammation and AHR, while autophagy activation in ILC2-specific TfebTG mice enhanced Th2 cytokine release, highlighting a central role for autophagy in the effector function and metabolic responses of ILC2s. This evidence concerns the gene ATG5 and inflammation.