Although, based on the current results it is difficult to ascertain the role of INPP4A in the pathophysiology of IPF, one way to reconcile our results is that fibrotic areas of the lung have burnt out inflammation and near‐complete EMT, while the adjacent non‐fibrotic areas have persisting inflammation and EMT changes which may explain the increase in INPP4A in non‐fibrotic regions of the fibrotic lungs either as an inducer of or a compensatory response during EMT. The gene discussed is INPP4A; the disease is idiopathic pulmonary fibrosis.