Subsection 5). The level of STAT3 in fibroblasts from patients with IPF correlates with progression of the disease. Small molecular inhibitors directed against STAT3 alleviate fibrosis in the mouse bleomycin model of IPF [55]. There is a strong association between STAT3 activation and oxidative-induced senescence, and this indicates a possible explanation for mitochondrial dysfunction in the pathogenesis of IPF [55]. The gene discussed is STAT3; the disease is idiopathic pulmonary fibrosis.