To further confirm this GBS-dependent response of CXCR4 promoter, we next generated artificial constructs containing four tandem copies of either a wild-type or mutated GBS, flanked by the thymidine kinase minimum promoter (TK pro), and examined whether these constructs responded to GLI1 and GLI2 in HEK293T cells, immortalized human mammary epithelial cells HMEC4hTertp16shRNA [33] (hereafter HMEC4tert), and HER2-type breast cancer cells SK-BR3. This evidence concerns the gene ERBB2 and breast carcinoma.