Wang, Hu, Chen and colleagues published in Nature Communications that mTORC1 signaling within group 2 innate lymphoid cells (ILC2s) mediates neuro-immune cross-talk driving allergic lung inflammation. The team mapped how neuronal inputs tune ILC2 metabolic programs via mTORC1 to amplify type 2 cytokine output. The study transparently links a metabolic regulator (mTORC1) to a discrete immune cell population and neural inputs, proposing mTORC1 as a tractable node for therapeutic modulation in allergic lung diseases. Authors discuss selective mTORC1 targeting to avoid systemic immunosuppression while dampening pathogenic neuro-immune loops.