The broad HDAC inhibitor TSA significantly decreased the level of TGF-β1 protein in radiation-induced type II AECs, inhibited their EMT important signaling pathways, and attenuated their EMT-like morphological changes by decreasing the expression of α-SMA, Snail, and E-calmodulin to attenuate the development of EMT-induced pulmonary fibrosis in AECs in radiation-associated ALI [193]. The gene discussed is SNAI1; the disease is pulmonary fibrosis.