Interestingly, transfection of IPF fibroblasts with a hyperactive HDAC1 mutant (actHDAC1), in which specific lysine residues were mutated to arginine (K218R, K220R, K432R, K438R, K439R, and K441R) to avoid AcK37, reduced the levels of the fibrosis markers (lanes 3–4) to levels similar to non-transfected Ctrl fibroblasts (compare lanes 4 and 1). The gene discussed is HDAC1; the disease is idiopathic pulmonary fibrosis.