In addition, we demonstrate that the protein stability of the phospho-dead mutant of BCL2L12 (T33A) is much higher than that of wild-type BCL2L12, and that the phospho-dead mutant of BCL2L12 has stronger ability to promote tumor formation in vivo than that of wild-type or phospho-mimic mutant, suggesting the importance of the regulatory roles of EYA1 on BCL2L12 in glioma development. This evidence concerns the gene BCL2L12 and glioma.