They showed that in BC cell lines with hyper-activated PI3K signalling, mTOR inhibition by rapamycin released the mTORC1-dependent suppression of insulin-like growth factor 1 receptor (IGF1R) and insulin receptor (IR), thus upregulating insulin receptor substrate 1 and restoring PI3K/AKT signalling[49]. This evidence concerns the gene AKT1 and breast cancer.