Entinostat (Ent), as a Class I HDAC inhibitor, downregulates pro-fibrotic genes Acta2 and Col1a1, as well as the pro-inflammatory factor LIF, by inhibiting the SRF-FOXM1 transcriptional axis at concentrations of 5–10 μM in vitro, thereby blocking CAF activation and weakening the STAT3 pathway in tumor cells (112). The gene discussed is HDAC9; the disease is neoplasm.