A known target of both SRC and AKT is the cell cycle inhibitor p27 (Figure 2); SRC and AKT indeed cooperate to inactivate the nuclear tumor suppressor activity of p27 in human cancers: SRC phosphorylates p27 at Tyr74 and Tyr88, thus accelerating its proteasome-mediated proteolysis [128], whereas AKT delays p27 nuclear import [129], promotes its degradation [130], and inhibits its transcription [131]. Here, AKT1 is linked to neoplasm.