Tumor necrosis factor α (TNF) has been shown to have potent antitumor activity, but its clinical use as an anticancer drug is hampered by its severe systemic toxicity. In this issue Curnis et al. (see p.1185) describe the generation of a modified TNF molecule bearing an N-terminal peptide that targets it to CD13, a cell surface molecule expressed on tumor vessels. The modified molecule induced stronger antitumor effects in vivo than TNF, at significantly lower doses, decreasing the tumor burden in lymphoma and melanoma animal models. Thus targeted delivery of TNF may enhance its therapeutic properties.