Gu et al. investigated the crosstalk between the complement, TGF-β1, and p38 in regulating CIP expression in the airway epithelium: (1) the expression level of CD46 and CD55 in lung tissue homogenates from patients with IPF was much lower compared to that of normal subjects, which resulted from their downregulation, especially in AECs and airway epithelia. The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.