The mice injected with lnc408-overexpressing non-BCSC had high rate of tumor initiation (Fig. 7A), which was compatible with the increased expression of nuclear β-catenin in the tumor (Fig. 7C); the mice injected with non-BCSC transfected with both ectopic lnc408 and CBY1 (non-BCSC/lnc408/CBY1) just had few tumor initiation (Fig. 7A), due to lowest nuclear β-catenin, which accompanied with high level of phosphorylated cytoplasm β-catenin, in the tumor (Fig. 7C), suggesting an essential role of lnc408/CBY1 axis in promoting tumor initiation of BCSCs via regulation of β-catenin signaling. The gene discussed is CBY1; the disease is neoplasm.