Knockout of PREX1 in cells from a second patient did not affect Lgl1 phosphorylation; these cells overexpressed a second Rac GEF, TIAM1, which was able to promote Lgl1 phosphorylation in the absence of PREX1, showing that there are redundant mechanisms for Lgl1 phosphorylation in a subset of glioblastoma patients. This evidence concerns the gene AKT1 and glioblastoma.