Given that (1) TTC3 induced by cigarette smoke extract caused cell death, possibly through the ubiquitylation and degradation of Akt17, (2) cigarette smoking is associated with idiopathic pulmonary fibrosis (IPF)22–24, (3) Akt inhibition ameliorated pulmonary fibrosis in bleomycin-treated mice25, and (4) Akt is one of the noncanonical signaling arms of TGF- β26 that is responsible in fibrotic changes in IPF27, we hypothesized that TTC3 might affect TGF-β-mediated EMT and myofibroblast differentiation, characteristic features of fibrotic diseases including IPF27. The gene discussed is AKT1; the disease is pulmonary fibrosis.