AKT1 and neoplasm: These dimers activate the tyrosine kinases, leading to autophosphorylation of tyrosine residues and triggering several downstream signaling pathways, including the Ras-Raf-mitogen-activated protein kinase pathway and the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway, which resulted in antiapoptosis, tumor cell proliferation, metastasis, and angiogenesis [66,67].