In support of this hypothesis, PI3K/AKT signalling, whose aberrant activation has been identified as crucial to the malignant features of glioblastomas, such as rapid tumour growth, invasiveness, and resistance to cytotoxic treatments [104], regulates sphingolipid metabolism, which promotes Cer vesicular transport and results in a reduction in ER Cer levels and increased synthesis of complex sphingolipids in glioma cells [105]. This evidence concerns the gene CBLN1 and central nervous system cancer.