In summary, the intricate pathogenesis of IPF (Figure 1) involves a dynamic interplay of factors, including TGF-β, IGF, CTGF, MMPs, exosomes, TNF-α, and interleukins, all contributing to the excessive production and deposition of ECM components, ultimately resulting in irreversible architectural distortion and loss of organ function. The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.