Specifically, we observed that Presenilin1 deficiency in high-grade glioma maintained persistent levels of cleaved Sortilin and promoted phosphorylation-degradation of β-catenin, while Presenilin1 repression released Sortilin and stabilized β-catenin, enhancing mesenchymal transition and increasing glioblastoma cell invasiveness (Fig. 8). The gene discussed is SORT1; the disease is glioma.