Furthermore, mouse xenograft experiments showed increased IGF-1R prosphorylation in CD45−/CD24−/CD44+ breast cancer stem cell (BCSC), while activation of the PI3K/AKT/mTOR pathway facilitated BCSC maintenance and increased their EMT phenotype indicating a regulatory role for the IGF-1R pathway in BrCa stem/progenitor cells [93]. This evidence concerns the gene IGF1R and breast carcinoma.