In human lung cancers, a population of CAFs has been isolated that expresses Thy-1, α-smooth muscle actin (αSMA), and fibroblast activation protein (FAP), but fails to express CD45 and CD11b, a phenotype consistent with that of an activated myofibroblast, and elicits either a contact-dependent enhancement or suppression of tumor-associated T cell activation12, 13. The gene discussed is ACTA1; the disease is lung cancer.