In agreement with our model, in which tumors are induced by activation of β-catenin and Bmpr1a mutations via the basal-specific K14-cre promoter16,17, we find that this trajectory initiates in basal tumor cells, further proceeds through the two CSC-like subpopulations, and ends in the luminal Clu+ cell cluster with continuous transitions in between (Fig. 5a, b). The gene discussed is CLU; the disease is neoplasm.