Regarding target engagement, the higher dose of cetuximab after repeated dosing than after a single dose in the H1975 tumors, the lack of EGFR protein degradation sustaining proliferative signaling in the less sensitive HCT116 tumors, and the similar lack of EGFR protein degradation in the H1975 model after gemcitabine monotherapy could explain the selective increase in tumor 18F-ICMT-11 uptake observed in the H1975 model after repeated dosing and combination therapy (Fig. 2; Supplemental Figs. 2 and 3). The gene discussed is EGFR; the disease is neoplasm.