Gliomas, in particular glioblastoma multiforme (GBM), are one of the most treatment-resistant tumours. GBM tumours frequently overexpress activated forms of several signaling molecules and the increased expression of these proteins correlates with adverse outcomes for patients in response to chemo- or radiation therapy, which result from the suppression of cell death (apoptosis) in these tumours. However, the mechanism of apoptotic resistance is not fully understood – yet it provides an unexplored opportunity to develop novel anticancer therapy. We have preliminary data indicating that the expression of several genes that modulate cell death program (antiapoptotic genes of the IAP and Bcl-2 protein families) are specifically upregulated in GBM. The reason for this is that another gene, called PDCD4, that normally renders expression of the antiapoptotic genes in check is lost in GBM. Interestingly, PDCD4 regulates protein synthesis of these antiapoptotic genes. We are interested in understanding the mechanism of how PDCD4 regulates expression of IAP and Bcl-2 protein families and exploiting this for the development of novel anticancer therapies.