Indeed, it has been hypothesized that factors associated with the more stem-like phenotype may account for CXCR4 expression in GBM [27], and we provided evidence that PATZ1 could be one of these factors: in VS-GB cells, a primary GBM cell line that does not express endogenous PATZ1, overexpression of PATZ1 leads to downregulation of CXCR4. Here, CXCR4 is linked to glioblastoma.