We confirmed both in our normal (Fig 6) and IPF (Fig 7) primary human cell strains that blocking FAK activity inhibited not only phosphorylation of Akt, but also expression of αSMA, confirming that FAK indeed regulates myofibroblast differentiation under normal and diseased conditions through activation of Akt pathway. The gene discussed is ACTA1; the disease is idiopathic pulmonary fibrosis.