EGFR and non-small cell lung carcinoma: Overexpression of OPN in NSCLC treated with EGFR-TKI compensated for the blockade of proliferation signals, causing EGFR-TKI-resistance.163 In the Ph+ CML cell lines, integrin β3 activated integrin-linked kinase (ILK) in response to extracellular signals, leading to imatinib resistance.164