This inconsistent correlation with the histological Nobiletin malignancy has already been found by other groups, even if Ki67 is often used to quantify the proliferative potential of gliomas in the clinical setting. Thus, our results show no correlation of Ki67 with KLF8 expression and as described earlier, Ki67 should therefore be interpreted with caution in the evaluation of proliferative activity of glial tumors of all WHO grades. Even if functional relevance of ML385 markers like Ki67 or KLF8 does not necessarily depend on protein or mRNA upregulation, deficient expression might still have an impact on cell proliferation. Hence, we subjected U87-MG cells to shRNA-knockdown of KLF8, which led to a significant time dependent impairment in their proliferation, providing first evidence for the potency of this transcription factor in human gliomas. This is in line with previous reports where inhibition of endogenous KLF8 by siRNA reduced cell cycle progression in NIH3T3 mouse fibroblasts. By targeting the downstream transcription molecule KLF8, we tried to exclude compensatory pathways which might counteract treatment effects on an upstream level. Yet, there is still a multitude of KLF8-related posttranscriptional regulations as described lately in non-malignant tissues; e.g. modulation of KLF8 transcriptional activity by co-activator proteins or by modification via acetylation. It now has to be elucidated whether KLF8 regulation follows similar mechanisms in glioma models in order to identify possible new key molecules. In summary, we have identified Kru��ppel-like factor 8 expression in the tumor parenchyma of human gliomas of different WHO grades without quantitative correlation to tumor grade or Ki67 expression. Inhibition of this potent transcription factor led to an almost complete loss of glioma cell proliferation in vitro, but its ubiquitous expression might counteract KLF8-targeting in malignant gliomas as a future antiproliferative strategy. Nevertheless, this work significantly advances our knowledge on glioma specific KLF8 expression patterns but independent functional relevance.