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]. This evidence concerns the gene IL2 and idiopathic pulmonary fibrosis.