We focused on Protein Tyrosine Phosphatase, Receptor Type R (PTPRR) here because it is well known to induce the dephosphorylation of ERK1/2, which plays an important role in the process of fibrotic response; it is also well known that the only drugs used in IPF (pirfenidone and nintedanib) exhibit anti-fibrotic effects by inhibiting tyrosine kinases [18]. The gene discussed is MAPK3; the disease is idiopathic pulmonary fibrosis.