Reports of ERα’s involvement in the activation of the epithelial–mesenchymal transition involved in GBM malignancy also seem relevant here [47], as 17β-estradiol and a selective ERα agonist induced an increase in the expression of mesenchymal markers such as vimentin and N-cadherin, and increased migration and invasion of GBM cells [47]. This evidence concerns the gene VIM and glioblastoma.