More recently, aberrant overexpression of GSK-3β has been shown to promote tumor growth and chemotherapy resistance in various solid tumors, including pancreatic, ovarian, colon cancer, and glioblastoma [16–20], through differential effects on pro-survival nuclear factor (NF)-κB and c-MYC pathways as well on tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and p53-mediated apoptotic mechanisms (Figure 1A) [21, 22]. This evidence concerns the gene GSK3B and neoplasm.