In summary, HDAC4 deacetylates KLF5 and increases its transcriptional activity to promote the expression of Slug and further upregulate CXCL12 expression, which causes the inflammation of bronchial epithelial cells and then induced the proliferation and migration of BSMCs, leading to airway remodeling, and thus facilitating the progression of asthma (Fig. 7). The gene discussed is HDAC4; the disease is asthma.