In addition to the NET-DNA-CCDC25 complex, studies using patient samples and xenograft models in the setting of breast cancer metastasis and bevacizumab-resistant invasive glioblastoma demonstrated ILK-dependent phosphorylation of c-Met, promoting ligand-independent receptor activation downstream of c-Met/β1-integrin complex formation [43] and high-affinity binding to fibronectin, allowing tumor cells to adapt to TME stressors such as hypoxia and bevaziumab exposure and drive chemotactic and haptotactic invasion [43]. Here, MET is linked to neoplasm.