EGFR mAbs are often more effective than TKIs, but resistance to these drugs in various carcinomas is also frequent and is mostly attributed to mutations of effectors downstream of RTKs such as Ras [132], phosphatidylinositol 3-kinase (PI3KCA) and/or loss of phosphatase and tensin homolog (PTEN) [133], as well as activation of BRAF [134]. Here, EGFR is linked to carcinoma.