Moreover, antitumour pasireotide-effects might be also explained by the observed decrease in key phosphoproteins involved in JAK/STAT-pathway, highlighting EGFR (important pathophysiological receptor in GBM [44]), the receptor JAK2, and other downstream intermediates, such as STAT6, whose relevance in GBM has been reported, promoting GBM cell-proliferation/migration/invasion [80]. This evidence concerns the gene SOAT1 and glioblastoma.