However, it is of note that a high concentration of insulin can lead to changes in the EMT phenotype of breast cancer cells via IGF1R.54 In addition, we found that these cell models derived from exocrine tissue required relatively higher doses of insulin to elicit response via IGF1R when compared to physiological insulin dose.19 This finding suggests the possibility that the pancreatic precursor cancer cells may react to physiological concentrations insulin via insulin receptor, and high levels of insulin would be expected to activate IGF1R. This evidence concerns the gene INSR and breast carcinoma.