In line with our previous findings that DBC1 enhances LEF1-β-catenin complex formation on WREs of β-catenin targets including a Wnt-inducible transcription factor PROX1 involved in colon cancer progression9, DBC1 increases LEF1-β-catenin interaction on the MACC1 enhancer, and loss of DBC1 reduced the occupancy of LEF1, TCF4, and β-catenin on the MACC1 enhancer. The gene discussed is PROX1; the disease is colonic neoplasm.