As expectedly, in comparison with BCSC with high level of endogenous lnc408, knockdown of lnc408 notably decreased tumorigenesis and tumor growth; while ectopic lnc408 in the non-BCSCs significantly promoted tumorigenesis and increased tumor growth, and the lnc408-droved tumor initiation was severely blunted by reexpression of CBY1 in non-BCSC (Fig. 7A). This evidence concerns the gene CBY1 and neoplasm.