To confirm whether the mechanism by which HNF1A-AS1 maintained stemness in xenograft tumor-bearing mice was consistent with the results observed in GC cells, we collected the tumors deriving from 2 × 105 dilution in vivo experiments and investigated the protein levels of β-catenin, CMYC, OCT4, SOX2, and NANOG in xenograft tumors formed by LV-HNF1A-AS1-transfected cells compared with control LV-NC-transfected cells. The gene discussed is SOX2; the disease is neoplasm.