Although the role of inflammation in the progression of IPF is in part controversial since some anti-inflammatory therapies have failed [31,32] to contrast the disease progression, it is well demonstrated that in fibrotic lungs, the population of lung macrophages are able to release high levels of pro-inflammatory cytokines, including IL-1β, TNF-α, and TGF-β, with the latter also having a crucial role in the induction of fibrosis [33,34]. The gene discussed is TNF; the disease is idiopathic pulmonary fibrosis.