Studies on a variety of cells—such as endothelial cells [79], MCF-7 breast cancer cells [80], and neurons [81–83]—have found that ERs can interact directly with PI3K or bind to the PI3K p85 subunit through scaffold proteins such as CAV-1, connective proteins such as Src and Shc, and growth factors, then activate the downstream Akt, causing a series of signal pathway cascades, such as the Akt-mTOR/JNK signal pathway [60–63]. This evidence concerns the gene MTOR and breast carcinoma.