Wang and colleagues found that the Y-box-binding protein 1 (YB-1) was strongly overexpressed in GBM tissues and cell lines, where it activated both mTORC1 and mTORC2 signaling pathways by increasing CCT4 production, which, in turn, promoted the mLST8 (MTOR-associated protein, LST8 homolog) folding and stability [114]. The gene discussed is CCT4; the disease is glioblastoma.