In multiple sclerosis, miR-34a was shown to be overexpressed in peripheral blood CD4+T lymphocytes, which resulted in decrease in suppressor of cytokine signaling 3 (SOCS3), leading to an increased production of cytokines and increase in Th17 cells.[36] Overexpression of miR-34a was also shown to play an imperative role in rheumatoid arthritis, by attenuating Foxp3 (phenotype marker of Treg cell) gene expression at the transcriptional level through targeting its 3’ UTR in CD4+ T cells.[36, 37] Besides, abnormal miR-34a expression has been reported in ILD. Here, FOXP3 is linked to interstitial lung disease.