Physiologically, variability results from non-specific agent uptake in normal tissues (i.e., non-specific binding in normal tissues with endogenously high EGFR expression like mucosa, salivary glands, and tonsils, and non-specific retention and perfusion of the agent caused by differences in vascular permeability) (23, 24) or from limited uptake in tumor tissues (i.e., not all HNSCCs overexpress EGFR due to heterogeneous gene expression, or complex, macroscopic structures reduce agent diffusion in regions of necrosis) (25). Here, EGFR is linked to neoplasm.