In previous studies, IL-1α was found to be elevated in a bleomycin-induced fibrosis model [71], and autoantibodies to this cytokine were also found in the serum of patients with rapidly progressive IPF [72], suggesting that IL-1α could play a significant role in the progression of IPF, and thus treatment with CM could contribute to its downregulation. The gene discussed is IL1A; the disease is idiopathic pulmonary fibrosis.