RB1 and neoplasm: The TIGAR inhibits the synthesis of cyclin-dependent kinase (CDK) complex members, resulting in the dephosphorylation of RB [20], and interacts with AKT to phosphorylate AKT and activate AKT, which subsequently mediates the PI3K-AKT-mTOR signaling pathway, thereby promoting tumor growth and metastasis, and inhibiting autophagy and apoptosis [21], as well as NF-kB signaling and inflammatory cytokines [22].