Furthermore, a comparison of BALF protein profiles between IPF patients, never-smoker healthy controls, and smoker controls using comparative two-dimensional gel electrophoresis (2D-PAGE) analysis revealed that transcription factors NF-kB, PPARγ, and c-MYC act as functional hubs, indicating the principal pathways involved in IPF progression and pathogenesis [42]. The gene discussed is PPARG; the disease is idiopathic interstitial pneumonia.