In cancer cells expressing kinase-activating mutations, the role of EGFR is shifted toward its kinase-dependent functions; while in cancer cells over-expressing wild type EGFR, the role of EGFR is shifted toward its kinase-independent functions; at situation of TKI treatment, the role of EGFR is also tilted toward its kinase-independent functions that allows cancer cells to survive and develop alternative growth-promoting mechanisms to counteract with TKI's inhibitory effect. Here, EGFR is linked to cancer.