The indirect activation of mTOR due to the phosphorylation of TSC complex subunit 2 (TSC2), an inhibitor of mTOR, as a result of AKT activation, can cause increased synthesis of cyclin D1, hypoxia-inducible factor 1 (HIF1) and vascular endothelial growth factor (VEGF), which can promote tumor progression. Here, AKT1 is linked to neoplasm.