Another study showed that under hypoxic conditions, HDAC3 interacts with hypoxia-induced WDR5, recruits the histone methyltransferase (HMT) complex to increase histone H3 lysine 4 (H3K4)-specific HMT activity, and activates mesenchymal gene expression [29], which is likely to contribute to pulmonary fibrosis. This evidence concerns the gene PRDM9 and pulmonary fibrosis.