Similarly, depletion of α2 or β1-integrin expression by hepatocellular carcinoma (HCC) cells in the context of IGF-1-driven signaling results in suppression of both ILK and FAK activity, leading to diminished activation of Akt/mTOR signaling and further indicating cooperative signal transduction by ILK and FAK downstream of integrins [69]. Here, MTOR is linked to hepatocellular carcinoma.