Since the expression of CCL2/MCP1 was shown to be higher in glioblastoma than in non-tumor tissue [34], and the NFκB and JNK pathways, well-known inflammatory signals, were found to be activated in GSCs [1,35], it is likely that the sustained activation of inflammatory signaling via high PLCε expression levels plays an important role in the initiation of glioblastoma. Here, CCL2 is linked to neoplasm.