The JIMT-1 model is unique because of displaying at the same time several co-existing mechanisms of resistance to trastuzumab present at variable levels in other breast cancer cell lines, including moderate expression levels of HER2 (despite HER2 gene amplification), low expression of PTEN (phosphatase and tensin homolog), an activating mutation of the PIK3CA gene, high expression of NRG1 (neuregulin-1), and enhanced expression of mesenchymal markers, including a naturally enriched subpopulation of breast cancer initiating CD44+CD24−/low CSC-like cells [2, 8-10]. This evidence concerns the gene PTEN and breast cancer.