In addition, we found that the overexpression of ASCL2 in CRC cells could mimic the effects conferred by L1 on cell proliferation, motility, tumorigenesis, and liver metastasis (including an elevation in the intestinal stem cell signature genes Lgr5, OLFM4, and SMOC-2), while ASCL2 suppression in L1-transfected CRC cells blocked these properties conferred by L1 [52]. The gene discussed is SMOC2; the disease is colorectal carcinoma.