Our study suggests that these same ER+ cells specifically respond to loss of RUNX1 function by E2-dependent downregulation of AXIN1, and that the mechanisms operative downstream of the RUNX1/AXIN1/β-catenin axis in these cells are distinct from those operative in Wnt-driven colon cancer and ER− breast cancer. The gene discussed is AXIN1; the disease is colonic neoplasm.