The activation of PR is known to increase proliferation, migration and invasion of GBM cells [26,27,28] through the transcription of essential factors for tumor growth, such as VEGF, cyclin D1 and EGFR [29]; however, it is unknown whether PR phosphorylation by PKC is through a direct or an indirect interaction and if this posttranslational modification results in activation of PR targets transcription. This evidence concerns the gene PGR and neoplasm.