Tumour angiogenesis is an important process in the development, growth and spread of tumours. There are several anti-angiogenic therapies currently used for cancer treatment, however these only extend the life of patients for a limited period of time due to the development of adaptive resistance and serious side-effects. Bone marrow (BM)-derived endothelial progenitor cells (EPCs) have been implicated as being essential in this process and important in the establishment of metastasis1 2 3 4 . Therefore, targeting these cells is critical to stopping tumour vasculature development and spread. In a previous study we have shown that the Inhibitor of DNA Binding 1 (ID1) proximal promoter can be used to silence genes in EPCs, thus resulting in decrease in EPC mobilization, tumour growth and angiogenesis2 . We have also demonstrated the vital role microRNAs, in particular, miR-10b in promoting bone marrow mediated tumour angiogenesis . In particular, we found using fluorescent in situ hybridization of human breast cancer biopsies, that miR-10b is localised to the vasculature of aggressive late stage invasive ductal carcinoma. Furthermore, we demonstrated that directed targeting of miR-10b to tumour vasculature using an anti-miRNA encapsulated in a RGD conjugated liposomes can significantly decrease tumour vascular development, growth and EPC mobilization1 . Recently, we have synthesized an EPC specific peptide and successfully conjugated this to liposomes. We are in the process of testing the ability of this peptide to direct nucleic acid therapy to EPCs in vivo. As this approach would direct the anti-miRNA therapy to EPCs, we believe this may lead to a novel anti-cancer therapy without problems associated with current therapies.