Also, pharmacologically co-targeting EGFR and SRC synergistically reduced the growth of CRIPTO1-positive, erlotinib-resistant, EGFRM+ NSCLC cells, suggesting that this combination might be able to counteract intrinsic resistance to EGFR-TKIs in patients with CRIPTO1-positive, EGFRM+ NSCLC undergoing EMT [215]. The gene discussed is CRIPTO; the disease is non-small cell lung carcinoma.