CDKN1B and glioblastoma: As discussed below, these dissimilarities could be also explained by the signaling pathways and mediators found in the present study to be differentially linked to sst5TMD4 overexpression in both GBM cells (e.g., overall activation of NF-κB-pathway [44,45], as well as the specific activation of CDKN1B [44] in U-87 MG cells).