Other studies in this area have focused on defining downstream components of signaling mediators following the initial mechanosensation event, and this has led to the identification YAP/TAZ, PHIP, and MGAT, among others that play a role in glioma stemness and disease progression; however, a unifying mechanism that considers heterogeneity in mechanical properties of the glioma microenvironment as well genetic and treatment-related drivers of plasticity is lacking and requires further investigation (96–104). The gene discussed is MGAT1; the disease is central nervous system cancer.