To understand whether, in human CRCs, the DREAM repression complex played a mechanistic role in causing the increased resistance of EpCAM+/CD44+/CD166+ (CSC-enriched) cancer cells to in vivo treatment with irinotecan (CPT-11), we decided to test whether E2F4 knock-down by short hairpin RNA (shRNA) constructs would translate in increased CRC sensitivity to the drug, across a variety of PDX lines (Supplementary Table 3). The gene discussed is EPCAM; the disease is cancer.