They observed that Treg depletion worsened the severity of AE-IPF, whereas IL-2 complex-induced expansion of Tregs leads to an attenuation, suggesting that Tregs could act as a regulator of the immune response during AE-IPF through downregulation of lung inflammatory cytokines, including TNF-α, IL-6, and TGF-β [107]. The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.