While their primary function is restraining autoimmunity through IL-10 and latent TGF-β production, in the chronic IL-6 rich environment characteristic of CTD-ILD, Tregs become impaired—driven by FOXP3 instability, increased STAT3 phosphorylation, and reduced suppressive capacity—rather than undergoing conversion into proinflammatory effector phenotypes [109,110,111,112]. This evidence concerns the gene FOXP3 and Autoimmunity.