Unfortunately, most monoclonal immunoglobulin-based therapies that inhibit function of HER2/neu, EGFR, VEGF, IGFR and other uniquely or highly over-expressed trophic receptors are usually only capable of promoting declines in proliferation rate and are largely incapable of evoking cytotoxic activity sufficient to effectively resolve most aggressive or advanced forms of neoplastic disease [7]–[12] [29]–[39]. Here, EGFR is linked to neoplasm.