This failure depends on several factors, including the complexity of the genetic alterations and tumor heterogeneity, the plasticity of tumor cells that enable them to activate alternative signalling pathways when one of them is antagonized, and the multiplicity of inflammatory molecules and growth factors from the stromal compartment, which might support EGFR-independent tumor cell growth and invasion [4, 20, 23, 39–41]. Here, EGFR is linked to neoplasm.