In contrast, treatment with an HDAC inhibitor, TSA (10 nmol/L), significantly reduced the viability of SMOi-resistant SI-CSC cells but did not affect isogenic vehicle-treated cells (Fig. 5F), indicating that reduced histone acetylation is critical to the survival of LDE225-treated SI-CSC medulloblastoma cells in vitro. This evidence concerns the gene HDAC9 and medulloblastoma.