The dependencies between PI3K/AKT and SOX2 however are reciprocal, as probably best exemplified in glioblastoma, where PI3K/AKT-imposed phosphorylation sustains nuclear SOX2 expression as a driving force of tumor cell dissemination, while in turn SOX2 supports PI3KCA gene expression (which actually locates in near juxtaposition of the SOX2 locus on chromosome band 3q26-28) and subsequent downstream activation of AKT [50]. Here, AKT1 is linked to neoplasm.