A different study showed that aSMase, but not nSMase, hydrolyzed sphingomyelin to generate ceramide and induced apoptosis in p53-deficient glioblastoma cells; while in p53 wild-type glioblastoma cells, p53 expression upregulated AC and blocked the ceramide response, thus allowing the cells to evade apoptosis. This evidence concerns the gene TP53 and glioblastoma.