Plasma and lung tissue from patients with IPF have increased levels of CTGF, which directs fibroblasts, epithelial cells, and alveolar macrophages to promote fibrogenesis.80, 81CTGF induces fibroblast proliferation and differentiation into myofibroblasts.82Both fibroblast-specific CTGF-deletion and inhibition using an anti-CTGF monoclonal antibody inhibited the development of bleomycin-induced fibrosis in mice.83, 84Targeted CTGF inhibition as a treatment modality for IPF is being approached through the development of novel monoclonal antibodies. This evidence concerns the gene CCN2 and fibrosis.