Wang, Hu, Chen and colleagues reported in Nature Communications that mTORC1 signaling within group 2 innate lymphoid cells (ILC2s) mediates neuro‑immune communication driving allergic lung inflammation. The study shows that neuronal signals engage mTORC1 in ILC2s to amplify type‑2 airway inflammation in preclinical models. By identifying mTORC1 as a nodal regulator of ILC2 responsiveness to neuropeptides, the work isolates a druggable intracellular pathway that could be explored for targeted interventions in severe asthma and other type‑2 inflammatory lung diseases.