Due to potential for complement-mediated lysis, ADCC and opsonization to all contribute to enhance the levels of anti-neoplastic cytotoxicity of covalent immunochemotherapeutics like gemcitabine-(C4-amide)-[anti-EGFR] and epirubicin-(C3-amide)-[anti-HER2/neu], it is technically very difficult to simultaneously and accurately simulate these three immune-dependent responses utilizing ex-vivo models for neoplastic disease. The gene discussed is EGFR; the disease is neoplasm.