Lu et al. (2001) reported that Herceptin resistance could occur through activation of IGF-IR. Other studies have indicated that co-targeting IGF-IR as well as ErbB2 would produce synergistic inhibition of growth in breast cancer cells (Camirand et al, 2002). Based upon our results as well as the results of these published studies, analysis of IGF-IR expression and downstream signalling may be critical for an accurate assessment of potential Herceptin response in breast cancer patients (right arm of Figure 2). This evidence concerns the gene IGF1R and breast carcinoma.