However, a bidirectional model showed glioma cells altering glial cells and regulating ERK, protein kinase B (Akt), and c-Jun N-terminal kinase (JNK) signaling pathways through paracrine interactions by the release of various proteins, including insulin-like growth factor-binding protein 2, myeloid-derived growth factors and metalloproteinase inhibitor 2 [90]. The gene discussed is AKT1; the disease is central nervous system cancer.