FRK and glioma: Rak also induces apoptosis and G1 arrest possibly through decreasing hyper-phosphorylated retinoblastoma (pRB) [34], a known interacting partner of Rak [26], and E2F1, and reduces migratory and invasive capabilities of glioma cells by suppressing the c-Jun N-terminal kinase (JNK)/c-Jun signaling pathway [36] and by enhancing the formation of the N-cadherin-β-catenin complex [37].