Furthermore, GL reduced phosphorylated GSK-3β (p-GSK-3β), but increased phosphorylation of Akt on serine 473 (p-Akt; Figure 3A, 3B), possibly due to a negative feedback mechanism, as observed earlier in various cancer cell lines treated with mTOR inhibitors such as everolimus [30] and rapamycin [31]. Here, AKT1 is linked to cancer.