We have previously demonstrated that in our tamoxifen resistant breast cancer cells, the IGF-1R can modulate pEGFR Tyr845 activity via mechanism dependent upon the non receptor tyrosine kinase c-Src (Knowlden et al, 2004) and furthermore, other studies have shown that in colon cancer cell lines with high IGF-1R expression, the IGF-1R can activate c-Src to modify cell transformation and motility (Sekharam et al, 2003). This evidence concerns the gene SRC and colonic neoplasm.