In agreement with the key role of SOX2 in glioma cancer stem cell renewal, and the reduction in SOX2 expression caused by shSIX1, knockdown of SIX1 had a clear functional impact in glioma cells, leading to a dramatic reduction of their self-renewal capacity, as measured by their ability to form oncospheres (Fig. 6c,f). This evidence concerns the gene SIX1 and central nervous system cancer.