SMYD2 and glioblastoma: At this respect, it has been recently reported that therapeutic inhibition of the constitutive activation of poly-ADP-ribose polymerase (PARP) compromises stem cell phenotypes and survival in glioblastoma-initiating cells.32 Interestingly, inhibiting PARP1 enhanced the cytotoxicity of DNA-damaging agents in cancer cells, and, more recently, it was shown that the activity of this enzyme was enhanced after its SMYD2-dependent methylation at Lys528,35 suggesting a functional link between the methylation status of CICs and their capacity to resist sublethal doses of radiation.