Targeted single-agent PTK therapies are effective in cancers where activation by mutation of one particular receptor is responsible for neoplastic progression (Druker et al, 2001; van Oosterom et al, 2001; Heinrich et al, 2002); however, in the more common situations where overexpression or deregulation of multiple PTKs are involved, combination approaches may prove to be of value and the IGF-1 receptor appears as a promising co-target. The gene discussed is PTK2B; the disease is cancer.