These findings confirm that the phenotypes observed in U-251 and UW479 ATRXKO clones are due to ATRX loss and not an off-target effect of CRISPR; in addition, these results have direct relevance to the current use of ATRX loss as assessed by immunohistochemistry as a diagnostic biomarker in glioma [56]. Here, ATRX is linked to central nervous system cancer.