To distinguish between these two possibilities, we used the remarkably synchronous and rapid in vivo Myc activation afforded by the MycERT2 switchable system (Christophorou et al., 2005, Littlewood et al., 1995, Pelengaris et al., 2002, Shchors et al., 2006, Wilson et al., 2014) to delineate the temporal sequence of events by which Myc activation drives transition to adenocarcinoma. The gene discussed is MYC; the disease is adenocarcinoma.