Using an RA-ILD mouse model, HDAC3 downregulated miR-19a-3p expression in the lung fibroblasts of these mice, which resulted in increased IL17/IL17RA signalling and ECM protein expression, an effect that was abrogated by overexpression of miR-19a-3p or siRNA-mediated Il17ra or Hdac3 silencing. Here, HDAC3 is linked to interstitial lung disease.