To pinpoint when the tumor progenitors first experience a TGFβ signal, where it comes from, and what the consequences are, Fuchs and colleagues (Oshimori et al. 2015) designed a lentivirus harboring a TGFβ-sensitive enhancer element to drive both mCherry and a CreER and then coupled it to a tetracycline-inducible skin tumorigenesis system. The gene discussed is TGFB1; the disease is neoplasm.