Based on these results, we proposed a transcriptional model where stable β-catenin controls colon cancer stemness and LGR5 expression through the enhancement of active Pol II complex formation by facilitating the formation of the Pol II–DSIF–NELF complex and the subsequent formation of the Pol II–DSIF–PAF1C complex (Fig. 6A). The gene discussed is LGR5; the disease is colonic neoplasm.